1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899
THE ATHLETE’S SHOULDER
ISBN: 978-0-443-06701-3
Copyright © 2009, 1994 by Churchill Livingstone, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail:
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on his or her experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher Library of Congress Cataloging-in-Publication Data The athlete’s shoulder/[edited by] Kevin E. Wilk, Michael M. Reinold, James R. Andrews. — 2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-0-443-06701-3 1. Shoulder—Wounds and injuries. 2. Sports injuries. I. Wilk, Kevin E. II. Reinold, Michael M. III. Andrews, James R. (James Rheuben). IV. Title. [DNLM: 1. Shoulder—injuries. 2. Athletic Injuries—therapy. 3. Rotator Cuff— injuries. 4. Shoulder Joint—injuries. WE 810 A871 2009] RD557. 5. A83 2009 617. 5’ 72044—dc22 2008002907
Acquisitions Editor: Daniel Pepper Developmental Editor: Angela Norton Publishing Services Manager: Frank Polizzano Project Manager: Jeff Gunning Design Direction: Lou Forgione
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Contributors
Robert Afra, M.D.
John C. Austin, M.D.
Assistant Professor, Chief of Sports Medicine, Department of Orthopaedic Surgery, University of California, San Diego, San Diego, California Mini-Open Rotator Cuff Repair
Northwest Orthopaedic Surgery and Sports Medicine, Hillsboro, Oregon Posterior Shoulder Instability
David W. Altchek, M.D.
Clinical Professor, Department of Physical Therapy, University of Delaware, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Michael J. Axe, M.D.
Attending Orthopaedic Surgeon, Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York Bankart Lesions: Diagnosis and Treatment with Arthroscopic and Open Approaches
David S. Bailie, M.D. Vice President, The Orthopedic Clinic Association, Scottsdale, Arizona Shoulder Arthroplasty in the Athletic Shoulder
Ammar Anbari, M.D. Orthopedic and Shoulder Surgery, Sports Medicine, Norwich Orthopedic Group, North Franklin, Connecticut Arthroscopic Rotator Cuff Repair
Champ L. Baker, Jr., M.D. Staff Physician, The Hughston Clinic, Columbus; Clinical Assistant Professor, Department of Orthopaedics, Medical College of Georgia, Augusta, Georgia Neurovascular Compression Syndromes of the Shoulder
James R. Andrews, M.D. Medical Director, The American Sports Medicine Institute; Clinical Professor of Surgery, Division of Orthopaedic Surgery, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama; Clinical Professor, Department of Surgery, University of South Carolina School of Medicine, Columbia, South Carolina; Clinical Assistant Professor, Department of Surgery, Florida State University College of Medicine, Tallahassee, Florida Operative Arthroscopy of the Shoulder; Internal Impingement; Open Repair of the Rotator Cuff; Shoulder Injuries in Baseball
Champ L. Baker III, M.D. Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Neurovascular Compression Syndromes of the Shoulder
Christopher W. Baker, M.D., M.P.H. Chief Resident, Department of Orthopedics, UMass Memorial Medical Center, Worcester, Massachusetts Tensile Failure of the Rotator Cuff; Shoulder Injuries in Football
Robert A. Arciero, M.D. Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine; Chief, Sports Medicine Division, Department of Orthopaedic Surgery, and Director, Orthopaedic Sports Medicine Fellowship Program, UConn Medical Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete
John-Erik Bell, M.D. Assistant Professor, Shoulder, Elbow, and Sports Medicine, Department of Orthopaedic Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Subacromial Impingement
J. Gregory Bennett, P.T., D.Sc., M.S. Peter D. Asnis, M.D.
Excel Physical Therapy, Fairfax; Adjunct Faculty, Advanced Orthopedics, Marymount University, Arlington, Virginia The Decelerator Mechanism: Eccentric Muscular Contraction Applications at the Shoulder
Instructor in Orthopaedic Surgery, Harvard Medical School; Assistant in Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Pediatric Shoulder Injuries v
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CONTRIBUTORS
Eric M. Berkson, M.D.
Richard B. Caspari, M.D. (deceased)
Clinical Associate Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Pediatric Shoulder Injuries
Clinical Professor, Division of Orthopedic Surgery, Virginia Commonwealth University Medical College of Virginia School of Medicine; Director, Orthopedic Research of Virginia, Richmond, Virginia Arthroscopic Techniques of the Shoulder
James Bicos, M.D. Orthopaedic Surgeon, Sports Medicine, St. Vincent Hospital, Minneapolis, Minnesota Management of the First-Time Shoulder Dislocation in the Athlete
Louis U. Bigliani, M.D.
Theresa A. Chiaia, B.S., B.S.P.T. Section Manager, Sports Rehabilitation and Performance Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
Attending Orthopaedic Surgeon, Columbia University Medical Center; Frank E. Stinchfield Professor and Chairman, Director of Orthopaedic Surgery Service, Chief of the Center for Shoulder, Elbow, and Sports Medicine, New York Presbyterian Hospital, New York, New York Subacromial Impingement
William G. Clancy, Jr., M.D.
James L. Bond, M.D.
The Center for Advanced Orthopaedics, Chillicothe, Ohio Arthroscopic Rotator Cuff Repair
Clinical Faculty, Department of Orthopedics, Division of Sports Medicine, University of Oklahoma; Orthopedic Surgeon, Oklahoma Sports and Orthopedics Institute, Norman, Oklahoma Partial Articular Supraspinatus Tendon Avulsion (PASTA) Lesions of the Rotator Cuff
Angie Botto-van Bemden, Ph.D. Director of Research, Uribe, Hechtman, Zvijac Sports Medicine Institute (UHZSMI), Coral Gables, Florida Multidirectional Instability of the Shoulder
Joe P. Bramhall, M.D. Director of Sports Medicine, Team Physician, Orthopedic Surgeon, Texas A&M Department of Athletics, College Station, Texas Operative Arthroscopy of the Shoulder
Brian D. Busconi, M.D.
Orthopaedic Surgeon, Andrews Sports Medicine Center, Birmingham, Alabama Soft Tissue Injuries of the Shoulder; Brachial Plexus Injuries
Brian S. Cohen, M.D.
David A. Cortese, M.D. Orthopedic Surgeon, Kaiser Permanente, Vancouver, Washington Superior Labral Anterior-Posterior Lesions of the Shoulder
Andrew J. Cosgarea, M.D. Professor, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine; Director, Division of Sports Medicine and Shoulder Surgery, Johns Hopkins Hospital, Baltimore, Maryland Suprascapular Nerve Entrapment
Ken Crenshaw, A.T.C., C.S.C.S., B.S. Head Athletic Trainer, Arizona Diamondbacks, Phoenix, Arizona Conditioning of the Shoulder Complex for Specific Sports
Associate Professor of Orthopedics and Physical Rehabilitation, University of Massachusetts Medical School; Chief of Sports Medicine, UMass Memorial Medical Center, Worcester, Massachusetts Tensile Failure of the Rotator Cuff; Shoulder Injuries in Football
Elsie Culham, P.T., Ph.D.
E. Lyle Cain, M.D.
Professor, Armstrong Atlantic State University, Savannah, Georgia; Professor Emeritus, University of Wisconsin– Lacrosse, Lacrosse, Wisconsin; Sports Physical Therapist, Gundersen Lutheran Sports Medicine, Lacrosse, Wisconsin, and Coastal Therapy, Savannah, Georgia The Shoulder in Swimming; Isokinetic Testing and Rehabilitation of the Shoulder Complex
Fellowship Director, American Sports Medicine Institute; Orthopaedic Surgeon, Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama Open Repair of the Rotator Cuff; Adhesive Capsulitis of the Shoulder; Shoulder Injuries in Baseball
William G. Carson, Jr., M.D. Assistant Professor of Orthopaedics, University of South Florida College of Medicine, Tampa, Florida Normal Arthroscopic Anatomy of the Shoulder
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Professor and Director, School of Rehabilitation Therapy, Queen’s University, Kingston, Ontario, Canada Functional Anatomy of the Shoulder Complex
George J. Davies, D.P.T., M.Ed., P.T., S.C.S., A.T.C., L.A.T., C.S.C.S., F.A.P.T.A.
Kathleen Devine, M.P.H., P.T. Owner, Advanced Health Systems, Sarasota, Florida Shoulder Injuries in Baseball
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CONTRIBUTORS
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David Donatucci, M.Ed.
Rafael Escamilla, Ph.D., P.T.
Human Performance Center, Bradenton, Florida Conditioning of the Shoulder Complex for Specific Sports
Professor, Department of Physical Therapy, California State University–Sacramento; Physical Therapist, Results Physical Therapy and Training Center, Sacramento, California Electromyographic Activity During Upper Extremity Sports; Open- and Closed-Chain Rehabilitation for the Shoulder Complex
Mark C. Drakos, M.D. Sports Medicine Fellow, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
Jeffrey R. Dugas, M.D. Orthopaedic Surgeon, Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama Internal Impingement
Shouchen Dun, M.S. Project Engineer, DePuy Orthopaedics, Inc., Warsaw, Indiana Biomechanics of the Shoulder During Sports
Brian J. Eckenrode, P.T., M.S.P.T., O.C.S. Advanced Clinician I, University of Pennsylvania Health System, Philadelphia, Pennsylvania Clinical Biomechanics of the Shoulder Complex
Sara L. Edwards, M.D. Orthopaedic Surgeon, Alta Bates Summit Medical Center, Oakland, California Subacromial Impingement
Marsha Eifert-Mangine, Ed.D., P.T., A.T.C. Assistant Professor, Department of Health Sciences, College of Mt. St. Joseph, Cincinnati, Ohio; Assistant Director of Research/Physical Therapist, NovaCare Rehabilitation, Florence, Kentucky Alternative Techniques for the Motion-Restricted Shoulder
Todd S. Ellenbecker, D.P.T., M.S., S.C.S., O.C.S., C.S.C.S.
Sue Falsone, P.T., M.S., S.C.S., A.T.C., C.S.C.S. Adjunct Professor, Department of Interdisciplinary Health Sciences, Arizona School of Health Sciences, A.T. Still University, Mesa; Director of Performance Physical Therapy, Athletes’ Performance, Core Performance, Tempe, Arizona Core Stabilization: Integration with Shoulder Rehabilitation
Glenn S. Fleisig, Ph.D. Adjunct Professor, Department of Biomedical Engineering, University of Alabama at Birmingham; Smith & Nephew Chair of Research, American Sports Medicine Institute, Birmingham, Alabama Biomechanics of the Shoulder During Sports
Michael B. Fox, B.A., B.S., P.T., S.C.S. Adjunct Faculty, New York University; Owner, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
Tandy R. Freeman, M.D. Orthopedic Surgeon, Mary Shiels Hospital, Dallas, Texas; Orthopedic Surgeon, Dallas Orthopedic Clinic, Dallas, Texas; Director of Medical Services, Justin Sports Medicine Team, Professional Rodeo Cowboys Association, Colorado Springs, Colorado; Medical Director, Professional Bull Riders, Inc., Pueblo, Colorado Brachial Plexus Injuries
Clinic Director, Physiotherapy Associates, Scottsdale, Arizona; Scottsdale Sports Clinic, National Director of Clinical Research, Physiotherapy Associates; and Director of Sports Medicine, APT Tour, Ponte Vedra Beach, Florida Shoulder Arthroplasty in the Athletic Shoulder; Shoulder Injuries in Tennis; The Shoulder in Swimming; Isokinetic Testing and Rehabilitation of the Shoulder Complex
Gregory Gebauer, M.D., M.S.
Matthew J. Ernst, M.P.T., O.C.S.
Adjunct Faculty, New York University; Owner, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
Adjunct Faculty, Physical Therapy Department, College of Mt. St. Joseph, Cincinnati, Ohio; Partner, Department of Physical Therapy, Oxford Physical Therapy Centers, Florence, Kentucky Alternative Techniques for the Motion-Restricted Shoulder
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Resident, Department of Orthopaedic Surgery, Johns Hopkins Hospital, Baltimore, Maryland Suprascapular Nerve Entrapment
William B. Geissler, M.D. University Orthopaedics, Jackson, Mississippi Arthroscopic Techniques of the Shoulder
Benjamin Gelfand, B.S., P.T., S.C.S.
Thomas J. Gill, M.D. Associate Professor of Orthopedic Surgery, Harvard Medical School; Chief, Sports Medicine Service,
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CONTRIBUTORS
Massachusetts General Hospital; Medical Director, Boston Red Sox; Head Team Physician, New England Patriots; Team Physician, Boston Bruins, Boston, Massachusetts Shoulder Injuries in Football; Pediatric Shoulder Injuries
Bruce Greenfield, P.T., Ph.D., O.S.C. Assistant Professor, Emory University, Atlanta, Georgia Proprioceptive Neuromuscular Facilitation for the Shoulder
Jo A. Hannafin, M.D., Ph.D. Professor of Orthopaedic Surgery, Weill Medical College of Cornell University; Attending Orthopaedic Surgeon and Orthopaedic Director, Womens Sports Medicine Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
Kevin Harmon, B.S. (Sports Medicine) Assistant Athletic Trainer, Texas Rangers Baseball Team, Arlington, Texas Conditioning of the Shoulder Complex for Specific Sports
Samer S. Hasan, M.D., Ph.D. Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
Richard J. Hawkins, M.D. Clinical Professor, Department of Orthopaedics, University of Colorado School of Medicine, Denver, Colorado, and University of Texas Southwestern Medical School, Dallas, Texas; Medical Director and Program Director, Steadman Hawkins Clinic of the Carolinas Fellowship, Steadman Hawkins Clinic of the Carolinas, Spartanburg, South Carolina Clinical Examination of the Shoulder Complex; Open Repair of the Rotator Cuff
Christopher Hughes, P.T., Ph.D., O.C.S., C.S.C.S Professor, School of Physical Therapy, Slippery Rock University, Slippery Rock; North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Airelle O. Hunter-Giordano, P.T., D.P.T., O.C.S., S.C.S., C.S.C.S. Clinical Faculty, Department of Physical Therapy, University of Delaware; Associate Director of Sports PT, University of Delaware Physical Therapy Clinic, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Wendy J. Hurd, P.T., Ph.D., S.C.S. Post-Doctoral Research Fellow, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
James J. Irrgang, Ph.D., P.T., A.T.C. Associate Professor and Director of Clinical Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine; Physical Therapist, Center for Sports Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Shoulder Outcome Measures
Ron M. Johnson, P.T., M.P.T., S.C.S., L.A.T., A.T.C., C.S.C.S. Facility Director, Excel Sports Therapy, Gulf Coast Rehabilitation, P.C., Shiner, Texas Conditioning, Training, and Rehabilitation for the Golfer’s Shoulder
Michael A. Keirns, Ph.D., P.T., S.C.S., A.T.C., C.S.C.S.
Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
Associate Professor, Regis University, Denver, Colorado; Facility Director and Senior Group Leader, Physiotherapy Associates at Greenwood Athletic Club, Greenwood Village, Colorado Nonoperative Treatment of Shoulder Impingement
Steven Hoffman, M.S., P.T., A.T.C., S.C.S.
Martin J. Kelley, P.T., D.P.T., O.C.S.
Clinical Instructor in Physical Therapy, Slippery Rock University, Slippery Rock, Pennsylvania; Chatham University; Washington University in St. Louis, St. Louis, Missouri; and West Virginia University, Morgantown, West Virginia; Owner, North Hills Orthopedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Musculoskeletal Team Leader, University of Pennsylvania Health System, Philadelphia, Pennsylvania Clinical Biomechanics of the Shoulder Complex
Timothy P. Heckman, P.T.
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W. Ben Kibler, M.D. Medical Director, Lexington Clinic Sports Medicine Center and Shoulder Center of Kentucky, Lexington, Kentucky The Role of the Scapula in Rehabilitation
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CONTRIBUTORS
David Kingsley, B.S. (BiomedEng)
Leonard C. Macrina, M.S.P.T., S.C.S., C.S.C.S.
Graduate Research Assistant, University of Southern Mississippi, Hattiesburg, Mississippi Biomechanics of the Shoulder During Sports
Physical Therapist, Champion Sports Medicine, Birmingham, Alabama Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Strength and Conditioning for the Preadolescent and Adolescent Athlete
Michael J. Kissenberth, M.D., B.S. (Biol) Assistant Clinical Professor of Orthopaedic Surgery and Medical Director, Orthopaedic Sports Medicine Service, Greenville Hospital System, Steadman Hawkins Clinic of the Carolinas, Greenville, South Carolina Clinical Examination of the Shoulder Complex
Stephen M. Kocaj, M.D. Department of Sports Medicine, Morristown Memorial Hospital, Morristown, New Jersey Adhesive Capsulitis of the Shoulder
Jeff G. Konin, Ph.D., A.T.C., P.T. Associate Professor, Department of Orthopaedic and Sports Medicine, University of South Florida College of Medicine; Executive Director, Sports Medicine and Athletic Related Trauma (SMART) Institute, Tampa, Florida Taping, Padding, and Bracing for the Shoulder Complex
Sanford S. Kunkel, M.D. Orthopaedic Surgeon, Indiana Orthopaedic Hospital, Indianapolis, Indiana Open Repair of the Rotator Cuff
Thomas J. Kuster III, M.S., A.T.C., N.A.S.M.-P.E.S. Assistant Athletic Director for Sports Medicine, James Madison University, Harrisonburg, Virginia Taping, Padding, and Bracing for the Shoulder Complex
David G. Lemak, M.D. Co-Director, Sports Medicine Fellowship, Lemak Sports Medicine, Brookwood Medical Center, Birmingham, Alabama Calcific Tendinitis
Lawrence J. Lemak, M.D. Director, Sports Medicine Fellowship, Lemak Sports Medicine, Brookwood Medical Center, Birmingham, Alabama Calcific Tendinitis
Scott M. Lephart, Ph.D., A.T.C. Associate Professor and Chair, Department of Sports Medicine and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Sensorimotor Contribution to Shoulder Joint Stability
Terry R. Malone, P.T., Ed.D., A.T.C., F.A.P.T.A. Professor, Department of Rehabilitation Sciences and Physical Therapy, University of Kentucky, Lexington, Kentucky Standardized Shoulder Examination—Clinical and Functional Approaches
Robert E. Mangine, M.Ed., P.T., A.T.C. Clinical Instructor, Department of Orthopedics, University of Cincinnati; Director of Sports Clinical Residency, NovaCare Rehabilitation, Cincinnati, Ohio Alternative Techniques for the Motion-Restricted Shoulder
Robert Manske, D.P.T., M.Ed., P.T., S.C.S., A.T.C., C.A.T., C.S.C.S. Associate Professor, Wichita State University; Sports Physical Therapist, Via Christi Medical Center, Wichita, Kansas The Shoulder in Swimming
James W. Matheson, D.P.T., M.S., P.T., S.C.S., O.C.S. Therapy Partners, Inc., Burnsville, Minnesota The Shoulder in Swimming
Augustus D. Mazzocca, M.S., M.D. Assistant Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine; Director of Clinical Biomechanics and Bioskills Laboratory, Department of Orthopaedic Surgery, UConn Health Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete; Acromioclavicular Joint Injuries
Mark D. Miller, M.D. Professor of Orthopaedic Surgery and Head, Division of Sports Medicine, University of Virginia, Charlottesville; Team Physician, James Madison University, Harrisonburg, Virginia Taping, Padding, and Bracing for the Shoulder Complex
Joseph B. Myers, Ph.D., A.T.C. Thomas N. Lindenfeld, M.D. Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
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Assistant Professor, Department of Exercise and Sport Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Sensorimotor Contribution to Shoulder Joint Stability
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CONTRIBUTORS
Larry Nassar, B.S., D.O. Associate Professor, College of Osteopathic Medicine, Department of Radiology, Division of Sports Medicine, Michigan State University, East Lansing, Michigan The Artistic Gymnast’s Shoulder
Stephen J. O’Brien, M.D., M.B.A Associate Professor of Orthopaedic Surgery, Weill Medical College of Cornell University; Associate Attending Orthopaedic Surgeon, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
Adam C. Olsen, P.T., A.T.C. Medical/Rehabilitation Coordinator, St. Louis Cardinals, Jupiter, Florida Interval Sport Programs for the Shoulder
Judson W. Ott, M.D. Orthopaedic Surgeon, Medical Associates, Dubuque, Iowa Soft Tissue Injuries of the Shoulder
Russell M. Paine, P.T., B.S. (Biol, PhysTher) Director of Rehabilitation, Memorial Hermann Sports Medicine; Team Physical Therapist, Houston Rockets, Houston, Texas Conditioning, Training, and Rehabilitation for the Golfer’s Shoulder
Christ J. Pavlatos, M.D.
Massachusetts General Hospital; Adjunct Faculty, Northeastern University College of Professional Studies, Boston, Massachusetts Internal Impingement; Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Strength and Conditioning for the Preadolescent and Adolescent Athlete; Biomechanical Considerations in Shoulder Rehabilitation Exercises; Interval Sport Programs for the Shoulder
Scott B. Reynolds, M.D. Orthopaedic Surgeon, Nebraska Orthopaedic Associates, Omaha, Nebraska Normal Arthroscopic Anatomy of the Shoulder; Operative Arthroscopy of the Shoulder; Arthroscopic Techniques of the Shoulder
Gordon Riddle, P.T., D.P.T., A.T.C., C.S.C.S. Adjunct Professor and Clinical Instructor, School of Physical Therapy, Slippery Rock University, Slippery Rock; Physical Therapist, North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Tara Ridge, M.S., P.T., S.C.S. UPMC Center for Sports Medicine, Pittsburgh, Pennsylvania Shoulder Outcome Measures
E. Paul Roetert, Ph.D.
Orthopaedic Surgeon, Libertyville, Illinois Acromioclavicular Joint Injuries
Managing Director, Player Development, United States Tennis Association, Boca Raton, Florida Shoulder Injuries in Tennis
Malcolm Peat, M.B.E., M.C.S.P., M.Sc., M.D. (Hon), Ph.D.
Anthony A. Romeo, M.D.
Executive Director of the International Centre for the Advancement of Community Based Rehabilitation (ICACBR), Faculty of Health Sciences, Queen’s University, Kingston, Ontario, Canada Functional Anatomy of the Shoulder Complex
Matthew Rappé, M.D. Knoxville Orthopaedic Clinic, Knoxville, Tennessee Open Repair of the Rotator Cuff
Jamie Reed, A.T.C. Head Athletic Trainer, Texas Rangers Baseball Team, Arlington, Texas Conditioning of the Shoulder Complex for Specific Sports
Michael M. Reinold, P.T., D.P.T., A.T.C., C.S.C.S. Rehabilitation Coordinator/Assistant Athletic Trainer, Boston Red Sox Baseball Team, Coordinator of Rehabilitation Research and Education, Department of Orthopedic Surgery, Division of Sports Medicine,
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Associate Professor of Orthopedics, Department of Sports Medicine, Rush University Medical Center, Chicago, Illinois Arthroscopic Rotator Cuff Repair
Omar Ross, B.S., M.S., P.T./D.P.T., A.T.C. Adjunct Professor and Clinical Instructor, School of Physical Therapy, Slippery Rock University, Slippery Rock; Physical Therapist, North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
J.R. Rudzki, M.D. Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York Bankart Lesions: Diagnosis and Treatment with Arthroscopic and Open Approaches
Stanley Rutkowski, B.S., B.A., P.T. Clinical Supervisor, New York University; Clinical Supervisor, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
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CONTRIBUTORS
Marc Safran, M.D. Professor of Orthopaedic Surgery and Associate Director, Sports Medicine, Stanford University, Stanford, California Shoulder Injuries in Tennis
William Sands, Ph.D., F.A.C.S.M., C.-A.R.S., N.R.E.M.T. Performance Services, U.S. Olympic Committee, Colorado Springs, Colorado The Artistic Gymnast’s Shoulder
Edgar T. Savidge, P.T., D.P.T., O.C.S. Senior Physical Therapist, MGH Sports Physical Therapy, Boston, Massachusetts Biomechanical Considerations in Shoulder Rehabilitation Exercises
Dorothy F. Scarpinato, M.D. Orthopaedic Surgeon, Central Orthopaedic Group, Plainview, New York Operative Arthroscopy of the Shoulder
Anthony Schepsis, M.D. Professor of Orthopedic Surgery, Boston University School of Medicine; Director of Sports Medicine, Boston University Medical Center, Boston, Massachusetts Mini-Open Rotator Cuff Repair
Martin L. Schwartz, M.D. Clinical Professor of Radiology, University of Alabama at Birmingham School of Medicine; Chairman, Department of Radiology, St. Vincent’s Birmingham, Birmingham, Alabama Diagnostic Imaging of the Shoulder Complex
Monique A. Sheridan, B.A. Medical Student, University of Maryland School of Medicine; Formerly Ludwig Research Fellow, Women’s Sports Medicine Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
James F. Silliman, M.D. President, Steadman Hawkins Clinic of the Carolinas; Program Medical Director, Musculoskeletal Institute of Greenville Hospital System, Greenville, South Carolina Clinical Examination of the Shoulder Complex
Stephen J. Snyder, M.D. Orthopedic Surgeon, Practice Limited to Shoulder Arthroscopy, Southern California Orthopedic Institute, Van Nuys, California Partial Articular Supraspinatus Tendon Avulsion (PASTA) Lesions of the Rotator Cuff; Superior Labral Anterior-Posterior Lesions of the Shoulder
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Lynn Snyder-Mackler, P.T., S.C.D., F.A.P.T.A., S.C.D. Alumni Distinguished Professor, Department of Physical Therapy, University of Delaware, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Samuel A. Taylor, M.D. Orthopaedic Surgery Resident, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
D. Dean Thornton, M.D. Clinical Assistant Professor of Radiology, Department of Radiology, University of Alabama at Birmingham; Musculoskeletal Radiologist, Radiology Associates of Birmingham PC, Birmingham, Alabama Diagnostic Imaging of the Shoulder Complex
Albert Tom, M.D. Sports Fellow, University of Connecticut, Farmington, Connecticut Acromioclavicular Joint Injuries
John Tomberlin, P.T., O.C.S., F.A.A.O.M.P.T. Director of Mercy SportsCare, Department of Rehabilitation Services, Mercy Medical Center, Cedar Rapids, Iowa Neurodynamic Techniques for the Athlete’s Shoulder
Tim L. Uhl, Ph.D. Associate Professor, Department of Rehabilitation Sciences, University of Kentucky College of Health Science, Lexington, Kentucky The Role of the Scapula in Rehabilitation
John Uribe, M.D. Professor and Chairman, Department of Orthopaedics, Florida International University, Miami, Florida Multidirectional Instability of the Shoulder
Nikhil N. Verma, M.D. Assistant Professor, Department of Orthopaedic Surgery, Rush Medical College, Chicago, Illinois Arthroscopic Rotator Cuff Repair
Mark Verstegen, B.S., M.S. Director of Performance, Player Safety, and Welfare, NFL Players Association; President and Founder, Athletes’ Performance, Andrews Institute/Home Depot Center, Arizona State University, Tucson; Creator, Core Performance System, Tempe, Arizona Core Stabilization: Integration with Shoulder Rehabilitation
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CONTRIBUTORS
Michael L. Voight, P.T., D.H.Sc., O.C.S., S.C.S., A.T.C., C.S.C.S. Professor, School of Physical Therapy, Belmont University, Nashville, Tennessee Plyometrics for the Shoulder Complex
Ilya Voloshin, M.D. Orthopaedic Surgeon, Boston University Medical School, Boston, Massachusetts Mini-Open Rotator Cuff Repair
Robert Y. Wang, M.D., F.R.C.S.C. York Central Hospital, Richmond Hill, Ontario, Canada Orthopaedic Sports Medicine Fellow, New England Musculoskeletal Institute, UConn Health Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete
Alabama; Adjunct Assistant Professor, Programs in Physical Therapy, Marquette University, Milwaukee, Wisconsin Functional Anatomy of the Shoulder Complex; Internal Impingement; Soft Tissue Injuries of the Shoulder; Adhesive Capsulitis of the Shoulder; Shoulder Injuries in Baseball; Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Isometric Testing and Rehabilitation of the Shoulder Complex; Plyometrics for the Shoulder Complex; Interval Sport Programs for the Shoulder
Kyle Yamashiro, P.T.
Craig A. Wassinger, Ph.D., P.T.
Medical Adjunct Faculty/Physical Therapist, Department of Athletics, California State University–Sacramento; Physical Therapist and CEO/Rehab Consultant, Oakland Athletics, Results Physical Therapy and Training Center, Sacramento, California Open- and Closed-Chain Rehabilitation for the Shoulder Complex
University of Otago, Dunedin, New Zealand Sensorimotor Contribution to Shoulder Joint Stability
Bashir Zikria, M.D.
Julie M. Whitman, D.Sc., M.P.T., B.S. (Biol) Assistant Professor, School of Physical Therapy, Regis University, Denver, Colorado Nonoperative Treatment of Shoulder Impingement
Kevin E. Wilk, P.T., D.P.T. Vice President Education, Physiotherapy Associates; Associate Clinical Director, Champion Sports Medicine, Physiotherapy Associates Clinic, Birmingham, Alabama; Rehabilitation Consultant, Tampa Bay Rays Baseball Team, Tampa Florida; Director Rehabilitation Research, American Sports Medicine Institute, Birmingham,
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Assistant Professor, Johns Hopkins Medicine, Lutherville, Maryland Multidirectional Instability of the Shoulder
John Zvijac, M.D. Professor, Department of Exercise Science and Sports Medicine, and Voluntary Associate Professor, Department of Orthopaedics/Rehabilitation, University of Miami Miller School of Medicine, Miami; Courtesy Professor, Department of Exercise and Sports Science, Florida International University, Miami; Team Physician, Tampa Bay Buccaneers, Tampa, Florida Multidirectional Instability of the Shoulder
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Preface
The shoulder joint continues to be one of the most intriguing joints in the human body. The interest in the shoulder joint in the orthopedic and sports medicine communities has stemmed from its functional and anatomic complexity, the precision of its biomechanics, and the wide variety of possible lesions affecting this structure. In the preface to the first edition of this textbook, we noted that increasing interest in the shoulder had led to “a proliferation of knowledge, enlightening research, improved awareness, and enhanced critical thinking regarding our recognition and treatment of shoulder joint disorders.” Since that time, almost 15 years ago, we have seen an even greater amount of interest and effort directed toward further understanding of the shoulder and its complex and intricate actions. The shoulder complex is a commonly injured region of the body, not only during sports but also as a result of work-related activities, overuse or disuse, and age-related degeneration. Accordingly, our goal in preparing this second edition was to make The Athlete’s Shoulder a comprehensive textbook addressing not only the most recent advances in sports-related shoulder disorders but also those occurring in the active orthopedic patient. Many iverse topics, including instabilities, labral lesions, rotator cuff lesions, neurovascular syndromes, total joint replacement, and biomechanics of specific sports, are discussed, and rehabilitation techniques are described in detail. Also included are several new chapters that overview current topics and recent advances in research in areas such as superior labral anterior-posterior (SLAP) tears, internal impingement, and articular-sided partial rotator cuff lesions. Several additional chapters are dedicated to various topics in surgery and rehabilitation. Each chapter has been updated and revised to contain the latest information available. This book is intended to not only increase the readers’ knowledge of the shoulder joint but also improve their understanding of the shoulder complex. The book is organized into six basic sections. The first, on the basic science of the shoulder complex, thoroughly discusses anatomy and biomechanics. This is followed by the examination section, which includes physical examination and diagnostic imaging of the shoulder. The third section describes recent arthroscopic surgical techniques. The fourth section discusses the recognition and treatment of various pathologies, including the appropriate surgical and rehabilitation approaches to these pathologies. The fifth section focuses on injuries in various sports and specific patient populations, such as baseball, golf, and the pediatric athlete. The last section discusses specific topics in rehabilitation. Although concise in format, the chapters provide the reader with a reference that includes historical perspective, functional anatomy, evaluation, and current treatment options. This text is not intended to be a “cookbook,” but rather is presented as a resource that enhances the practitioner’s expertise in the examination and treatment of shoulder injuries. The way we think about and look at the shoulder has changed over the years, and we are sure that this trend will continue. The challenge has been to prepare a text that discusses current and advanced concepts in an area in which knowledge is expanding daily. It is our hope that this book meets this challenge—and that it enables the reader to look into the future of shoulder treatment. We hope that this second edition of The Athlete’s Shoulder stimulates interest, provokes thought, inspires additional research, and enhances the care of shoulder patients in the future. We offer this textbook to clinicians, physicians, physical therapists, athletic trainers, and others involved in caring for shoulder patients. May it help you to discover more about the enormously fascinating shoulder joint, a truly complex functional structure that, once you begin exploring, becomes even more intriguing and complex in its interrelationships. The contributors to this book represent the leaders in shoulder care, and we greatly appreciate their contributions. Their work in the fields of orthopedics and sports medicine related to the shoulder has been invaluable to the continued advancement of understanding and treatment of shoulder pathology. Kevin E. Wilk, P.T., D.P.T. Michael M. Reinold, P.T., D.P.T., A.T.C., C.S.C.S. James R. Andrews, M.D.
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Acknowledgments
To Kevin Wilk, Glenn Fleisig, and Jim Andrews: Your mentorship, guidance, and friendship have been an invaluable gift to me. You have served as excellent role models and engraved in me the values of work ethic, team work, and leadership. I can’t thank you enough for sharing your knowledge and helping me to open so many doorways. To my family, especially Sandi, Mom, Dad, Lance, and Lucy: Thank you for your love, encouragement, patience, and understanding throughout my life. By following the values you have instilled and examples you have set, I have always been provided with motivation needed for me to be my best. Your strength and perseverance through life’s ups and downs continue to provide a driving force in everything I do, even from a distance. To all my past students, colleagues, patients, and players: Thank you for supplying the motivation to challenge myself to further my understanding of the shoulder. To everyone at Elsevier who was involved with this project, especially Jeff Gunning, Julia Bartz, and Angela Norton: This book would not have happened without your help and persistence.
Michael M. Reinold
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CHAPTER 1 Functional Anatomy of the
Shoulder Complex Malcolm Peat, Elsie Culham, and Kevin E. Wilk
The glenohumeral joint is the most complex joint in the human body. The glenohumeral joint combined with the scapulothoracic, sternoclavicular, and acromioclavicular joints comprise the shoulder joint complex. All these joints are critical to normal pain-free function. The glenohumeral joint has the greatest amount of motion of any joint in the human body.
COMPONENTS Sternoclavicular Joint The sternoclavicular joint is the only joint connecting the shoulder complex to the axial skeleton.9,10 Although the structure of this synovial joint is classified as plain, its function most closely resembles a ball-and-socket articulation.4,11,12 The articular surfaces lack congruity. Approximately one half of the large, rounded medial end of the clavicle protrudes above the shallow sternal socket. An intra-articular disc is attached to the upper portion of this nonarticular segment of the clavicle. The articular surface is saddle-shaped, anteroposteriorly concave, and downwardly convex.2,4
The overall function of the upper extremity is related to the shoulder complex, with the ultimate purpose of this mechanism being the placement and full use of the hand. The joint mechanisms of the limb permit the placement, functioning, and control of the hand directly in front of the body, where the functions can be observed.1 Manipulation of the hand is controlled by the shoulder complex, which positions and directs the humerus, the elbow, which positions the hand in relation to the trunk, and the radioulnar joints, which determine the position of the palm.2,3 Sports that involve actions such as throwing, using a racket, and swimming require excessive glenohumeral joint motion. For example, the excessive motion required to throw a baseball is accomplished through the integrated and synchronized motion of the various joints in the upper quadrant, most significantly the glenohumeral and scapulothoracic joints.
The medial end of the clavicle is bound to the sternum, the first rib and its costal cartilage. Ligaments strengthen the capsule anteriorly, posteriorly, superiorly, and inferiorly. The main structures stabilizing the joint, resisting the tendency for medial displacement of the clavicle and limiting clavicular movement, are the articular disc and the costoclavicular ligament (Fig. 1-1).4,13 The articular disc is a strong, almost circular fibrocartilage that completely divides the joint cavity.14 The disc is attached superiorly to the upper medial end of the clavicle and passes downward between the articular surfaces to the sternum and first costal cartilage.4 This arrangement permits the disc to function as a hinge, a mechanism that contributes to the total range of joint movement. The areas of compression between the articular surfaces and intraarticular disc vary with movements of the clavicle. During elevation and depression, most motion occurs between the clavicle and articular disc (Fig. 1-2A and B). During protrusion and retraction, the greatest movement occurs between the articular disc and sternal articular surface (see Fig. 1-2C and D).2 The combination of taut ligaments, pressure on the disc and articular surfaces is important for maintaining stability in the plane of motion.
The shoulder complex provides the upper limb with a range of motion exceeding that of any other joint mechanism.4 This range of motion is greater than that required for most daily functional activities. For example, use of the hand in limited activities of daily living is possible when the shoulder complex is immobilized with the humerus held by the side. Compensation for absent shoulder motion is provided by the cervical spine, elbow, wrist, and finger joint mechanisms.5,6 The shoulder complex consists of four joints that function in a precise, coordinated, synchronous manner. Position changes of the arm involve movements of the clavicle, scapula, and humerus. These movements are the direct result of the complex mechanism comprised of the sternoclavicular, acromioclavicular, and glenohumeral joints and the scapulothoracic gliding mechanism.4,7,8
The articular disc also stabilizes the joint against forces applied to the shoulder, which are transmitted medially through the clavicle to the sternum. Without this attachment, the 3
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THE ATHLETE’S SHOULDER
The joint capsule is supported by oblique anterior and posterior sternoclavicular ligaments. Both ligaments pass downward and medially from the sternal end of the clavicle to the anterior and posterior surfaces of the manubrium and limit anteroposterior movement of the clavicle. An interclavicular ligament runs across the superior aspect of the sternoclavicular joint, joining the medial ends of the clavicles. This ligament, with deep fibers attached to the upper margin of the manubrium, provides stability to the superior aspect of the joint.4,9
Clavicle
Disc
The sternoclavicular joint allows elevation and depression, protraction and retraction, and long-axis rotation of the clavicle. The axis for both angular movements lies close to the clavicular attachment of the costoclavicular ligament.9 Costoclavicular ligament
Acromioclavicular Joint
Figure 1-1. Sternoclavicular joint showing major ligamentous structures influencing stability.
clavicle would tend to override the sternum, resulting in medial dislocation. Forces acting on the clavicle are most likely to cause fractures of the bone medial to the attachment of the coracoclavicular ligament but rarely cause dislocation of the sternoclavicular joint.5 The costoclavicular ligament is a strong bilaminar structure attached to the inferior surface of the medial end of the clavicle and first rib. The anterior component of the ligament passes upward and laterally; the posterior aspect upward and medially. The ligament is a major stabilizing structure and strongly binds the medial end of the clavicle to the first rib. The ligament becomes taut when the arm is elevated or the shoulder protracted.4
The acromioclavicular joint is a synovial plane joint between the small, convex, oval facet on the lateral end of the clavicle and a concave area on the anterior part of the medial border of the acromion process of the scapula.4,9 The joint line is oblique and slightly curved. The curvature of the joint permits the acromion, and thus the scapula, to glide forward or backward over the lateral end of the clavicle. This movement keeps the glenoid fossa continually facing the humeral head. The oblique nature of the joint is such that forces transmitted through the arm will tend to drive the acromion process under the lateral end of the clavicle, with the clavicle overriding the acromion (Fig. 1-3). The joint also contains a fibrocartilaginous disc that is variable in size and does not completely separate the joint into two compartments.9,14 The acromioclavicular joint is
Taut ligament
Taut ligament
Contact Contact
Depression
Elevation
B
A
Taut ligament Figure 1-2. Sternoclavicular joint illustrating compression of articular disc. A, Depression. B, Elevation. C, Retraction. D, Protrusion. (From Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49, 1965.)
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Contact
Contact
Taut ligament
C
Retraction
D
Protrusion
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
5
The primary function of this ligament is to prevent overriding of the clavicle on the acromion.5,17
Acromion
Clavicle
Figure 1-3. Acromioclavicular joint surfaces.
important because it contributes to total arm movement in addition to transmitting forces between the clavicle and acromion.4,15 The acromioclavicular joint has a capsule and superior acromioclavicular ligament that strengthen the upper aspect of the joint.4,11 The main ligamentous structure stabilizing the joint and binding the clavicle to the scapula is the coracoclavicular ligament. Although this ligament is placed medially and is separate from the joint, it forms the most efficient means of preventing the clavicle from losing contact with the acromion.4,5,8,9,15,16 The coracoclavicular ligament consists of two parts, the trapezoid and the conoid. These two components, functionally and anatomically distinct, are united at their corresponding borders. Anteriorly, the space between the ligaments is filled with adipose tissue and, frequently, a bursa. A bursa also lies between the medial end of the coracoid process and the inferior surface of the clavicle. In up to 30% of subjects, these bony components may be opposed closely and may form a coracoclavicular joint.2,16 The coracoclavicular ligament suspends the scapula from the clavicle and transmits the force of the upper fibers of the trapezius to the scapula.2 The trapezoid ligament, the anterolateral component of the coracoclavicular ligament, is broad, thin, and quadrilateral. It is attached from below to the superior surface of the coracoid process. The ligament passes laterally almost horizontally in the frontal plane and is attached to the trapezoid line on the inferior surface of the clavicle.4,9
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The conoid ligament is located partly posteriorly and medially to the trapezoid ligament. It is thick and triangular, with its base attached from above to the conoid tubercle on the inferior surface of the clavicle. The apex, which is directed downward, is attached to the “knuckle” of the coracoid process (i.e., medial and posterior edge of the root of the process). The conoid ligament is oriented vertically and twisted on itself.4,17 The ligament limits upward movement of the clavicle on the acromion. When the arm is elevated, the rotation of the scapula causes the coracoid process to move and increases the distance between the clavicle and coracoid process. This movement increases the tension on the conoid ligament, resulting in dorsal (posterior) axial rotation of the clavicle. Viewed from above, the clavicle has a shape resembling a crank. The taut coracoclavicular ligament acts on the outer curvature of the cranklike clavicle and effects a rotation of the clavicle on its long axis.11,18 This clavicular rotation allows the scapula to continue to rotate and increase the degree of arm elevation. During full elevation of the arm, the clavicle rotates 50 degrees axially.11 When the clavicle is prevented from rotating, the arm can be abducted actively to only 120 degrees.4,8 Movement of the acromioclavicular joint is an important component of total arm movement. A principal role of the joint in the elevation of the arm is to permit continued lateral rotation of the scapula after about 100 degrees of abduction when sternoclavicular movement is restrained by the sternoclavicular joint ligaments. The acromioclavicular joint has three degrees of freedom. Movement can occur between the acromion and lateral end of the clavicle about a vertical axis, around a frontal axis, or about a sagittal axis. Functionally, the two main movements at the acromioclavicular joint, however, are a gliding movement as the shoulder joint flexes and extends and an elevation and depression movement to conform with changes in the relation between the scapula and humerus during abduction.5,9,16
Glenohumeral Joint The glenohumeral joint is a multiaxial ball-and-socket synovial joint. This type of joint geometry permits a tremendous amount of motion; however, the inherent stability is minimal (Fig. 1-4). The articular surfaces, head of the humerus, and glenoid fossa of the scapula, although reciprocally curved, are oval and are not sections of true spheres.4 Because the head of the humerus is larger than the glenoid fossa, only part of the humeral head can be in articulation with the glenoid fossa in any position of the joint. At any given time, only 25% to 30% of the humeral head is in contact with the glenoid fossa.19-21 The surfaces are not congruent, and the joint is loose-packed. Full congruence and the close-packed position are obtained when the humerus is in full elevation.22,23
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THE ATHLETE’S SHOULDER
Other investigators have also reported bilateral differences in retroversion in overhead athletes, in whom the throwing side exhibits greater retroversion.27-29 The glenoid fossa is somewhat pear-shaped and resembles an inverted comma (Fig. 1-5). The surface area is 25% to 33%, the vertical diameter 75%, and the transverse diameter 55% of that of the humeral head.25 In 75% of subjects, the glenoid fossa is retroverted an average of 7.4 degrees in relation to the plane of the scapula.30,31 Furthermore, the glenoid fossa has a slight upward tilt of about 5 degrees in reference to the medial border of the scapula32; we refer to this as the inclination angle. It has been suggested that this relation is important in maintaining horizontal stability of the joint and counteracting any tendency toward anterior displacement of the humeral head.25,30,31 However, this concept has not been supported by subsequent studies.33,34 The articular cartilage lining the glenoid fossa is thickest in the periphery and thinnest in the central region. Figure 1-4. Osseous structure of the glenohumeral joint. The large convex humeral head is in a relatively small glenoid fossa.
The design characteristics of the joint are typical of an incongruous joint. The surfaces are asymmetrical, the joint has a movable axis of rotation, and muscles related to the joint are essential in maintaining stability of the articulation (Box 1-1).9 The humeral articular surface has a radius of curvature of 35 to 55 mm. The humeral head and neck make an angle of 130 to 150 degrees with the shaft and are retroverted about 20 to 30 degrees with respect to the transverse axis of the elbow.24,25
Because of the amount of pathology involving the acromion and head of the humerus, the acromion has been studied extensively. Bigliani and Morrison35 have classified the shapes of the acromion into three categories. Type I acromions are those with a flat undersurface and have the lowest risk for impingement syndrome and its sequelae. Type II acromions have a curved undersurface and type III acromions have a hooked undersurface (Fig. 1-6). Type III has the highest correlation with impingement syndromes, rotator cuff pathologies or both. Nicholson and associates36 have reported that the shape of the acromion is congenital and does not develop over time. The acromions have epiphysis and occasionally may not fuse, leading to acromion deformity, often referred to as os acromiale.37
The topic of retroversion has received increased attention because of the implications of its effect on glenohumeral joint motion. Nowhere is this point more evident than with the overhead athlete, who exhibits excessive external rotation and a limitation of internal rotation. Crockett and colleagues26 have studied professional baseball pitchers and noted a bilateral difference in humeral retroversion. The investigators noted a 17-degree difference, with the throwing shoulder exhibiting greater external rotation and loss of internal rotation. This difference was not observed in the control group of non–overhead throwing athletes. Box 1-1. Stability
Factors Contributing to Glenohumeral
Osseous configuration (joint geometry) Glenoid labrum Glenohumeral capsule Neuromuscular system Negative intra-articular pressure
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Figure 1-5. Lateral view of the glenoid fossa. Note the pear-shaped appearance and similarity to an inverted comma.
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
A
7
increase the depth of the concave surface substantially, and that the glenoid labrum is no more than a fold of capsule composed of dense fibrous connective tissue that stretches out anteriorly with external rotation and posteriorly with internal rotation of the humerus.40 The main function of the labrum may be to serve as an attachment for the glenohumeral ligaments.4,40 When that attachment is compromised, it represents a Bankart lesion, in which the capsular-labral complex is detached from the glenoid rim (Fig. 1-7; see Fig. 1-6).
Capsule
B
C Figure 1-6. Acromial shapes. A, Type 1, flat acromion. B, Type II, curved acromion. C, Type III, hooked acromion.
The resting position of the scapula in reference to the trunk is anteriorly rotated about 30 to 40 degrees,21,38 with respect to the frontal plane as viewed from above. This has been referred to as the scapular plane. The scapula is also rotated upward about 3 degrees and tilted forward approximately 20 degrees.38,39
The capsule surrounds the joint and is attached medially to the margin of the glenoid fossa beyond the labrum. Laterally, it is attached to the circumference of the anatomic neck, and the attachment descends about 1⁄2 inch onto the shaft of the humerus. The capsule is loose-fitting, allowing the joint surfaces to be separated 2 to 3 mm by a distractive force.4 Matsen and colleagues42 have shown 22 mm of inferior, 6 mm anterior, and 7 mm posterior translation in normal subjects. The capsule is relatively thin and, by itself, would contribute little to the stability of the joint. The integrity of the capsule and maintenance of the normal glenohumeral relationship depend on the reinforcement of the capsule by ligaments and attachment of the muscle tendons of the rotator cuff mechanism.4,9,16 The superior part of the capsule, together with the superior glenohumeral ligament, is important in strengthening
Glenoid Labrum The glenoid labrum consists of fibrocartilage and fibrous tissue.4,40 This rim of fibrocartilaginous tissue attaches around the margin of the glenoid fossa.40 The inner surface of the labrum is covered with synovium; the outer surface attaches to the capsule and is continuous with the periosteum of the scapular neck. The shape of the labrum adapts to accommodate rotation of the humeral head, adding flexibility to the edges of the glenoid fossa. The tendons of the long head of the biceps brachii muscle contribute to the structure and reinforcement of the labrum. The long head of the biceps brachii attaches to the superior region of the labrum. The width and thickness of the glenoid labrum vary. The anterior labrum appears thicker and at times larger than the posterior labrum. It has been suggested40 that the labrum protects the edges of the glenoid, assists in lubrication of the joint, and deepens the glenoid cavity, thus contributing to stability of the joint.4,5,9,41 Others have stated that the labrum does not
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A
B Figure 1-7. Capsular-labral complex defect, often described as a Bankart lesion. A, Lateral capsular flap reattached to glenoid rim. B, Added strength from double-breasting the medial capsule, reinforcing the entire glenoid rim from 2:00 to 6:00.
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THE ATHLETE’S SHOULDER
the superior aspect of the joint and resisting the effect of gravity on the dependent limb.4,43 Anteriorly, the capsule is strengthened by the anterior glenohumeral ligaments and attachment of the subscapularis tendon (Fig. 1-8).44 Posteriorly, the capsule is strengthened by the attachment of the teres minor and infraspinatus tendons.45 Inferiorly, the capsule is relatively thin and weak and contributes little to the stability of the joint. The inferior part of the capsule is subjected to considerable strain because it is stretched tightly across the head of the humerus when the arm is elevated. The inferior part of the capsule, the weakest area, is lax and lies in folds when the arm is adducted. Kaltsas46 has compared the collagen structure of the shoulder joint capsule with that of the elbow and hip. When the joint capsules were subjected to a mechanical force, the shoulder joint capsule showed a greater capacity to stretch than to rupture. When the capsule was tested to failure, the structure ruptured anteroinferiorly.46,47 Also, Reeves47 has demonstrated that the force required to cause glenohumeral joint dislocation is less in those younger than 20 years and greater in those older than 50 years. O’Brien and coworkers48 have described the glenohumeral capsule and its ligamentous structures and noted that the anterior capsule is comprised of three ligamentous portions—the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament complex (IGHLC) (Fig. 1-9). The IGHLC is comprised of the anterior band (AB), posterior band (PB), and axillary pouch (AP). The study noted that during abduction and external rotation, the anterior band acts as a hammock, resulting in anterior displacement of
Coracohumeral
Superior glenohumeral
Middle glenohumeral Inferior glenohumeral
Figure 1-8. Coracohumeral and glenohumeral ligaments. Note the deficiencies between the glenohumeral ligaments and the Z arrangement of the three components of the ligament.
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B SG HL P
M G H
PC
A L
A B
PB AP IG H L C
Figure 1-9. Glenohumeral joint capsule. Note the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament complex (IGHLC). AB, anterior band; AP, axillary pouch; PB, posterior band.
the humerus (see Fig. 1-9). Conversely, with abduction internal rotation, the posterior band functions as a ligamentous restraint to posterior displacement. The axillary pouch functions as a redundancy to the capsule, allowing excessive mobility. Fealy and colleagues49 have examined the glenohumeral joint in 51 fetal shoulders ranging from 9 to 40 weeks of gestation. The authors noted distinct capsules with ligaments present, especially a prominent inferior glenohumeral ligament complex. A coracohumeral ligament and rotator cuff interval were also present. Johnston23 has stated that, with the arm by the side, the capsular fibers are oriented with a forward and medial twist. This twist increases in abduction and decreases in flexion. The capsular tension in abduction compresses the humeral head into the glenoid fossa. As abduction progresses, the capsular tension exerts an external rotation moment. This external rotation untwists the capsule and allows further abduction. The external rotation of the humerus that occurs during coronal plane abduction may therefore be assisted by the configuration of the joint capsule.23 The capsule is lined by a synovial membrane attached to the glenoid rim and anatomic neck inside the capsular attachments.4 The tendon of the long head of the biceps brachii muscle passes from the supraglenoid tubercle over
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
the superior aspect of the head of the humerus and lies within the capsule, emerging from the joint at the intertubercular groove (Fig. 1-10). The tendon is covered by a synovial sheath to facilitate movement of the tendon within the joint. The structure is susceptible to injury at the point at which the tendon arches over the humeral head, and the surface on which it glides changes from bony cortex to articular cartilage.5
TABLE 1-1 Stability of the Glenohumeral Joint Position
Structure
Dependent
Coracohumeral ligament Superior glenohumeral ligament Supraspinatus muscle
Elevation (degrees) Lower range (0-45)
Coracohumeral Ligament The coracohumeral ligament is an important ligamentous structure in the shoulder complex.43 The ligament is attached to the base and lateral border of the coracoid process and passes obliquely downward and laterally to the humerus, blending with the supraspinatus muscle and the capsule. Laterally, the ligament separates into two components that insert into the greater and lesser tuberosities, creating a tunnel through which the biceps tendon passes.50 Inferiorly, the coracohumeral ligament blends with the superior glenohumeral ligament. The anterior border of the ligament is distinct medially and merges with the capsule laterally. The posterior border is indistinct and blends with the capsule.4,9 It has been suggested that the downward pull of gravity on an adducted arm is counteracted largely by the superior capsule, coracohumeral ligament, and inferior glenohumeral ligament (Table 1-1).50,51 As the arm is abducted, the restraining force is shifted to the inferior structures and the primary restraining force is the inferior glenohumeral ligament.52 Because the coracohumeral ligament is located anteriorly to the vertical axis about which the humerus rotates axially, the ligament checks lateral rotation during arm elevation between 0 and 60 degrees. When
9
Anterior capsule Superior glenohumeral ligament Coracohumeral ligament Middle glenohumeral ligament Subscapularis, infraspinatus, and teres minor muscles
Middle range (45-75) Middle glenohumeral ligament (MGHL) Supscapularis muscle (decreasing importance) Infraspinatus and teres minor muscles Inferior glenohumeral ligament (superior band) Upper range (⬎75)
Inferior glenohumeral ligament (anterior band; axillary pouch)
Throughout elevation Dynamic activity of rotator cuff
the humerus, in a position of neutral rotation, is elevated in the sagittal plane, the movement is limited to approximately 75 degrees by the coracohumeral ligament. For elevation to continue, the humerus is medially rotated and moves toward the scapular plane by the dynamic tension in this ligament.22
Glenohumeral Ligaments The three glenohumeral ligaments lie on the anterior and inferior aspect of the joint . They are described as being thickened parts of the capsule.4 The superior glenohumeral ligament passes laterally from the superior glenoid tubercle, upper part of the glenoid labrum, and base of the coracoid process to the humerus, between the upper part of the lesser tuberosity and anatomic neck.50,51 The ligament lies anterior to and partly under the coracohumeral ligament. The superior glenohumeral ligament, together with the superior joint capsule and rotator cuff muscles, assist in preventing downward displacement of the humeral head.51,53
Anterior
Medial
Figure 1-10. Attachments of the glenohumeral ligaments to the humerus.
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The middle glenohumeral ligament has a wide attachment, extending from the superior glenohumeral ligament along the anterior margin of the glenoid fossa down as far as the junction of the middle and inferior thirds of the glenoid rim.51 From this attachment, the ligament passes laterally, gradually enlarges, and attaches to the anterior aspect of the anatomic neck and lesser tuberosity of the humerus. The ligament lies under the tendon of the subscapularis muscle and is intimately attached to it.25,50 Note
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THE ATHLETE’S SHOULDER
the large variation in size of the middle glenohumeral ligament; it can be 2 cm wide but is absent in some individuals. This structure exhibits the greatest amount of structural variation. The middle glenohumeral ligament and subscapularis tendon limit lateral rotation from 45 to 75 degrees of abduction and are important anterior stabilizers of the glenohumeral joint, particularly effective in the lower to middle ranges of abduction (see Table 1-1).
Inside the glenohumeral joint capsule is negative pressure in comparison with outside the joint capsule. This is referred to as negative intra-articular pressure and provides a stabilizing effect on the shoulder joint.54 Wulker and colleagues55 have demonstrated that venting the capsule (creating a cut into the capsule, thus eliminating the negative intra-articular pressure) may increase translation of the humerus on the glenoid by 19% to 50%.
The inferior glenohumeral ligament is the thickest of the glenohumeral structures and is the most important stabilizing structure of the shoulder in the overhead athlete. The ligament attaches to the anterior, inferior, and posterior margins of the glenoid labrum and passes laterally to the inferior aspects of the anatomic and surgical necks of the humerus.4,25 The ligament can be divided into three distinct portions—the anterior band, axillary pouch, and posterior band (see Fig. 1-9).48 The inferior part is thinner and broader and is termed the axillary pouch. The anterior band strengthens the capsule anteriorly and supports the joint most effectively in the upper ranges (more than 75 degrees) of abduction.48 The anterior band of the inferior glenohumeral ligament provides a broad buttresslike support for the anterior and inferior aspects of the joint, preventing subluxation in the upper part of the range (see Table 1-1).51
Rotator Cuff: Dynamic Stability
O’Brien and associates48 have demonstrated that with the arm abducted to 90 degrees and externally rotated, the anterior band of the inferior glenohumeral ligament complex wraps around the humeral head like a hammock to prevent anterior humeral head migration. This structure provides stability during the throwing motion, tennis serve motion, freestyle stroke, or any overhead arm position. Tightening of the inferior glenohumeral ligament during coronal plane abduction limits elevation to an average of 90 degrees. To continue to elevate, the humerus must move toward the scapular plane and laterally rotate. Gagey and coworkers22 have stated that both movements occur because of dynamic tension in the inferior glenohumeral ligament. The coracohumeral and glenohumeral ligaments viewed from the front form a Z pattern . This arrangement creates potential areas of capsular weakness above and below the middle glenohumeral ligament. The subscapularis bursa communicates with the joint cavity through the superior opening, or foramen of Weitbrecht, between the superior and middle glenohumeral ligaments. Ferrari50 has also reported the presence of an inferior subscapular bursa, between the middle and inferior glenohumeral ligaments. This bursa was present in all 14 specimens in those younger than 55 years and could be seen up to the age of 75 years. When the middle glenohumeral ligament is attenuated or absent, this anterior defect is enhanced and may contribute to anterior instability of the joint.50
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The rotator cuff is the musculotendinous complex formed by the attachment to the capsule of the supraspinatus muscle superiorly, the subscapularis muscle anteriorly, and the teres minor and infraspinatus muscles posteriorly. These tendons blend intricately with the fibrous capsule and the adjacent rotator cuff tendon.56 They provide active support for the joint and can be considered true dynamic ligaments that provide dynamic stability.8 The capsule is less well protected inferiorly because the tendon of the long head of the triceps brachii muscle is separated from the capsule by the axillary nerve and posterior circumflex humeral artery.4 The rotator cuff tendons insert into a large contact point onto the greater and lesser tuberosities of the humerus and not a small insertion point, as was once thought. Dugas and associates57 have reported that the rotator cuff inserts less than 1 mm from the articular margin. Curtis and coworkers58 later reported that the insertional anatomy in cadaveric shoulders exhibits a consistent pattern and noted interdigitation of the muscles, particularly between the supraspinatus and infraspinatus. The average insertional lengths and widths for the rotator cuff muscles were as follows: supraspinatus 23 ⫻ 16 mm, subscapularis 40 ⫻ 20 mm, infraspinatus 29 ⫻ 19 mm, and teres minor 29 ⫻ 11 mm. Bassett and colleagues59 have studied the cross-sectional area of the rotator cuff muscles as they cross the glenohumeral joint capsule (Table 1-2); they found that the larger the cross-sectional area, the more significant the contribution to shoulder stability. Miller and associates60 have described a space between the supraspinatus and infraspinatus and referred to this area as the posterior rotator cuff interval. They went on to discuss the importance of releasing this area when rotator cuff repairs are performed in specific types of patients who exhibit supraspinatus retraction and scarring. It is generally accepted that the deltoid and the rotator cuff muscles are prime movers of glenohumeral abduction.61-63 These muscles have been found to contribute equally to torque production in functional planes of motion.63 With the arm at the side, the directional force of the deltoid muscle is almost vertical.25,64 Thus, most of the deltoid force will cause a superior shear force of the humeral head that, if unopposed, would cause the humeral head to contact the coracoacromial arch, resulting in impingement of soft
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
TABLE 1-2 Cross-Sectional Area of Rotator Cuff Muscles Crossing the Glenohumeral (GH) Joint Capsule
Muscle
Contribution of Muscle Area (cm2) Crossing GH Joint (%)
Biceps (LH)
2.01
2
Biceps (SH)
1.11
2
Deltoid
18.2
17.7
5.0
5
Infraspinatus and teres minor
13.7
13
Latissimus dorsi
12.0
11.7
Pectoralis major
13.3
13
Subscapularis
16.3
16
Supraspinatus
5.7
5.6
Teres major
8.77
8.5
Triceps
3.0
3.8
Deltoid (posterior)
From Bassett R, Browne A, Morrey BF, et al: Glenohumeral muscle force and moment mechanics in a position of shoulder instability. J Biomech 23:405, 1990.
tissues.65 The force vectors of the infraspinatus, subscapularis, and teres minor muscles are such that each tends to have a compressive component as well as a rotational force.39,65 Each muscle’s compressive force offsets the superior shear force of the deltoid.39 The infraspinatus, teres minor, and subscapularis thus form a force coupled with the deltoid and act to stabilize the humeral head on the glenoid fossa, allowing the deltoid and supraspinatus to act as abductors of the humerus.66 We often refer to the rotator cuff muscles as the compressive cuff. In studies on a mechanical model, Comtet and coworkers61 have determined that the depressor forces are at their maximum between 60 and 80 degrees of elevation and disappear beyond 120 degrees. The supraspinatus has a small superior shear component, but its main function is compression because of the horizontal orientation of the muscle fibers39; thus, it opposes the upward superior shear action of the deltoid. Lesions of the rotator cuff mechanism can occur as a response to repetitious activity over time or to overload activity that causes a spontaneous lesion.67 Stress applied to a previously degenerated rotator cuff may cause the cuff to rupture. Often, this stress also tears the articular capsule, resulting in a communication between the joint cavity and subacromial bursa. Rotator cuff tears result in considerably reduced force of elevation of the glenohumeral joint. In attempting to elevate the arm, the patient shrugs the shoulder. If the arm is abducted passively to 90 degrees, the patient should be able to maintain the arm in the abducted position.9
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11
The space between the supraspinatus and superior border of subscapularis has been termed the rotator interval. This space is triangular, with its base located medially at the coracoid process. The rotator interval contains the coracohumeral ligament, superior glenohumeral ligament, glenohumeral capsule, and biceps tendon.68-72 The medial aspect consists of two layers and the lateral portion is composed of four layers. The superficial layer of the medial rotator interval is comprised of the coracohumeral ligament and the deep layer consists of the superior glenohumeral ligament and joint capsule. The coracohumeral ligament also represents the superficial layer of the lateral portion of the rotator interval. The second layer is composed of the fibers of the supraspinatus and subscapularis. The third layer consists of the deep fibers of the coracohumeral ligament and the fourth layer is the superior glenohumeral ligament and lateral capsule.68,69 The size of the rotator cuff interval varies. The larger the interval, the greater the inferior and posterior laxity.72 The function of the long head of the biceps is controversial. Some believe that it contributes to the stability of the glenohumeral joint by preventing upward migration of the head of the humerus during powerful elbow flexion and forearm supination. Lesions of the long head of the biceps, therefore, may produce instability and shoulder dysfunction.73 Conversely, other physicians74-76 have reported performing biceps tenotomy in patients with refractory biceps pain. Once the biceps was released, pain was eliminated in over 70% of patients and no functional limitations, instability, or weakness were reported. Thus, the function of the proximal long head of the biceps brachii is still being debated. The scapula plays a vital role in normal shoulder function. Normal scapulothoracic joint motion and rhythm are critical to pain-free normal shoulder function. Numerous muscles about the scapula play a critical role in accomplishing this function. The trapezius muscle is the largest and most superficial scapulothoracic muscle. This muscle originates from the spinous processes of the C7 through T12 vertebrae. The muscle is classified into upper, middle, and lower fibers. Insertion of the upper fibers is over the distal third of the clavicle. The lower cervical and upper thorax fibers insert over the acromion and spine of the scapula. The lower portion of the trapezius inserts into the base of the spine of the scapula. The rhomboids function similarly as the midportion of the trapezius.77 The origin of the rhomboids is from the lower ligamentum nuchae, C7 and T1 for the rhomboid minor and T2 through T5 for the rhomboid major. The rhomboid minor inserts onto the posterior portion of the medial base of the spine of the scapula. The rhomboid major inserts onto the medial border of the scapula. The levator scapulae muscle proceeds from its origin on the transverse processes from C1 through C3 (and sometimes C4) and inserts onto the superior angle of the scapula. The serratus anterior takes its origin from the ribs on the lateral wall of the thoracic cage.
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THE ATHLETE’S SHOULDER
The serratus has three divisions, upper, middle and lower. The upper fibers originate from ribs 1 and 2, the middle fibers from ribs 2 through 4, and the lower from ribs 5 through 9. The serratus anterior muscle orientation is in individual slips from each rib. The serratus inserts onto the superior angle, medial border, and inferior angle of the scapula, respectively. The pectoralis minor runs from the second through fifth ribs upward to the medial base of coracoid. Somewhat frequently, approximately 15% incidence, there will be an aberrant slip from the pectoralis minor to the humerus, glenoid, clavicle, or scapula.78,79 The subclavius muscle is a small muscle that originates from the first rib and inserts as a muscle onto the inferior surface of the medial third of the clavicle. This muscle stabilizes the sternoclavicular joint.
Coracoacromial Arch The coracoacromial ligament is triangular with the base attached to the lateral border of the coracoid process (Fig. 1-11). The ligament passes upward, laterally, and slightly posteriorly to the superior aspect of the acromion process.4,80 Superiorly, the ligament is covered by the deltoid muscle. Posteriorly, the ligament is continuous with the fascia that covers the supraspinatus muscle. Anteriorly, the coracoacromial ligament has a sharp, well-defined, free border. Together with the acromion and the coracoid processes, the ligament forms an important protective arch over the glenohumeral joint.9 The arch forms a secondary restraining socket for the humeral head, protecting the joint from trauma from above and preventing upward
dislocation of the humeral head. The supraspinatus muscle passes under the coracoacromial arch, lies between the deltoid muscle and the capsule of the glenohumeral joint, and blends with the capsule. The supraspinatus tendon is separated from the arch by the subacromial bursa (see Fig. 1-11).9 The space between the inferior acromion and head of the humerus (subacromial distance) has been measured on radiographs and is used as an indicator of proximal humeral subluxation.81,82 The distance was found to be between 9 and 10 mm in 175 asymptomatic shoulders and was greater in men than in women.81 A distance of less than 6 mm was considered pathologic and was thought to be indicative of supraspinatus tendon attenuation or rupture.81 During elevation, with internal rotation of the arm in abduction and flexion, the greater tuberosity (the supraspinatus tendon) of the humerus may apply pressure against the anterior edge and inferior surface of the anterior third of the acromion and coracoacromial ligament. This is in part because of the anterior orientation of the supraspinatus tendon. In some cases, the impingement also may occur against the acromioclavicular (AC) joint. This often occurs when the AC joint exhibits degenerative joint disease or spurring, or both. Most upper extremity functions are performed with the hand placed in front of the body, not lateral to it. When the arm is raised forward in flexion, the supraspinatus tendon passes under the anterior edge of the acromion and acromioclavicular joint. For this movement, the critical area for wear is centered on the supraspinatus tendon and also may involve the long head of the biceps brachii muscle. Flatow and colleagues83 have examined the concept of impingement, compression between the supraspinatus and acromion. The investigators measured the distance between the undersurface of the acromion and humeral head at various degrees of abduction. At 0 degrees adduction (arm at the side), the acromiohumeral space was approximately 11 mm, at 90 degrees of abduction it was 5.7 mm, and at 120 degrees of abduction less than 5 mm (4.8 mm). Furthermore, the investigators placed Fuji contact film, which measures pressure per square area, on the acromion and humeral head. They found that with arm abduction from 60 degrees to full elevation, there was contact between the acromion and humeral head. Therefore, Flatow and associates83 have reported that contact between the humeral head and acromion is normal.
Bursae
Figure 1-11. Coracoacromial ligament and its relation to the humeral head.
Ch01_001-016-F06701.indd 12
Several bursae are found in the shoulder region.4 Two bursae particularly important to the clinician are the subacromial and subscapular bursae.15 Other bursae located in relation to the glenohumeral joint structures are between the infraspinatus muscle and capsule, on the superior surface of the acromion, between the coracoid process and
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
capsule, under the coracobrachialis muscle, between the teres major and long head of the triceps brachii muscles, and in front of and behind the tendon of the latissimus dorsi muscle. Because bursae are located where motion is required between adjacent structures, they have a major function in the shoulder mechanism. The subacromial bursa (Fig. 1-12) is located between the deltoid muscle and capsule, extending under the acromion and coracoacromial ligament and between them and the supraspinatus muscle. The bursa adheres to the coracoacromial ligament and to the acromion above and rotator cuff below. The bursa does not frequently communicate with the joint; however, a communication may develop if the rotator cuff is ruptured.80 The subacromial bursa is important for allowing gliding between the acromion and deltoid muscle and rotator cuff. It also reduces friction on the supraspinatus tendon as it passes under the coracoacromial arch.9,80 Often, with repetitive overhead motion, the bursae may become inflamed and thickened, which may decrease the critical space in the subacromial region. The subscapular bursa lies between the subscapularis tendon and neck of the scapula. It protects this tendon where it passes under the base of the coracoid process and over the neck of the scapula. The bursa communicates with the joint cavity between the superior and middle glenohumeral ligaments9,51 and often between the middle and inferior glenohumeral ligaments.40,50
Vascular Supply The rotator cuff is a frequent site of pathologic conditions, usually degenerative and often in response to fatigue stress.17 Because degeneration may occur even with normal activity levels, the nutritional status of the glenohumeral structures is of great importance. The blood supply to the Acromion
Deltoid Subacromial bursa Supraspinatus
13
rotator cuff comes from the posterior humeral circumflex and suprascapular arteries.4 These arteries supply principally the infraspinatus and teres minor muscle areas of the cuff. The anterior aspect of the capsular ligamentous cuff is supplied by the anterior humeral circumflex artery and occasionally by the thoracoacromial, suprahumeral, and subscapular arteries. Superiorly, the supraspinatus muscle is supplied by the thoracoacromial artery. The supraspinatus tendon has a region of relative avascularity 1 cm proximal to the humeral insertion, often including its insertion into the humerus.84,85 Rothman and Parke85 have reported hypovascularity in the tendon in 63% of 72 shoulders studied. In a study by Rathbun and MacNab,84 an avascular area was found in all specimens and was unrelated to age. Abduction of the arm resulted in relaxation of the tension on the supraspinatus muscle and complete filling of vessels throughout the tendon. In addition, with increasing age, the area of avascularity also increases67; thus, the potential for healing decreases with age. The other cuff tendons generally demonstrate good vascularity, except for an occasional zone of hypovascularity in the superior portion of the insertion of the infraspinatus tendon.84,85
Articular Neurology Innervation of the shoulder region is derived from C5, C6, and C7; C4 also may add a minor contribution. The nerves supplying the ligaments, capsule, and synovial membrane are axillary, suprascapular, subscapular, and musculocutaneous nerves. Branches from the posterior cord of the brachial plexus also may supply the joint structures. Occasionally, the shoulder may receive a greater supply from the axillary nerve than from the musculocutaneous nerve; the reverse may also be true. The complex overlapping innervation pattern makes denervation of the joint difficult. The nerve supply follows the small blood vessels into periarticular structures.4,5 The skin on the anterior region of the shoulder complex is supplied by the supraclavicular nerves from C3 and C4 and by the terminal branches of the sensory component of the axillary nerve. The articular structures on the anterior aspect of the glenohumeral joint are supplied by the axillary nerve and, to a lesser degree, by the suprascapular nerves. The subscapular nerve and posterior cord of the brachial plexus may also innervate the anterior aspect of the joint after piercing the subscapularis muscle.4,5,9 The supraclavicular nerves supply the skin on the superior and upper posterior aspects of the shoulder region. The lower, posterior, and lateral aspects of the shoulder are supplied by the posterior branch of the axillary nerve.
Figure 1-12. Supraspinatus tendon and related structures.
Ch01_001-016-F06701.indd 13
The periarticular structures on the superior aspect of the joint obtain part of their innervation from the suprascapular nerve. The axillary and musculocutaneous nerves
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14
THE ATHLETE’S SHOULDER
and the lateral pectoral nerve may also contribute to the innervation of the superior aspect of the joint. Posteriorly, the main nerve supply is from the suprascapular nerve, which supplies the proximal part of the joint, and the axillary nerve, which supplies the distal region.3-5,9 The acromioclavicular joint is innervated by the lateral supraclavicular nerve from the cervical plexus (C4) and by the lateral pectoral and suprascapular nerves from the brachial plexus (C5 and C6). The sternoclavicular joint is innervated by branches from the medial supraclavicular nerve from the cervical plexus (C3 and C4) and subclavian nerve from the brachial plexus (C5 and C6).4,9
SUMMARY The shoulder complex is more mobile than any other joint mechanism of the body because of the combined movement at the glenohumeral and scapulothoracic articulations. This wide range of motion permits positioning of the hand in space, allowing performance of numerous gross and skilled functions. Shoulder complex stability is also required during dynamic activity, particularly when the distal extremity encounters resistance. The glenohumeral joint is inherently unstable because of the shallowness of the glenoid fossa as well as the disproportionate size and lack of congruency between the articular surfaces. During dynamic activities, stabilization of the humeral head on the glenoid fossa depends on an intact capsule and glenohumeral ligaments, as well as on coordinated and synchronous activity in the deltoid and rotator cuff muscles. Injury or disease of any of these structures can lead to instability and impingement of subacromial structures, resulting in pain and dysfunction in the shoulder region.
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35. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228, 1986. 36. Nicholson GP, Goodman DA, Flatow EL: The cromion: Morphologic condition and and age-related changes. A study of 420 scapulas. J Shoulder Elbow Surg 5:1, 1996. 37. Lieberson F: Os acromiale—a contested anomaly. J Bone Joint Surg 19:683, 1937. 38. Laumann U: Kinesiology of the Shoulder Joint. In Kolbel R (ed): Shoulder Replacement. Berlin, Springer-Verlag, 1987. 39. Morrey BF, An KN: Biomechanics of the shoulder. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, p 235. 40. Moseley HF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder: Morphological and clinical studies with special reference to the glenoid labrum and the gleno-humeral ligaments. J Bone Joint Surg Br 44:913, 1962. 41. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247, 1983. 42. Matsen FA, Harryman DT, Didles JA: Mechanics of glenohumeral instability. In Hawkins RJ (ed): Clinics in Sports Medicine: Basic Science and Clinical Application in the Athlete’s Shoulder. Philadelphia, WB Saunders, 1991. 43. Basmajian JV, Bazant FJ: Factors preventing downward dislocation of the adducted shoulder joint. J Bone Joint Surg Am 41:1182, 1959. 44. Ovesen J, Nielsen S: Anterior and posterior shoulder instability: A cadaver study. Acta Orthop Scand 57:324, 1986. 45. Ovesen J, Nielsen S: Posterior instability of the shoulder: A cadaver study. Acta Orthop Scand 57:436, 1986. 46. Kaltsas DS: Comparative study of the properties of the shoulder joint capsule with those of other joint capsules. Clin Orthop 173:20, 1983. 47. Reeves B: Experiments on the tensile strength of the anterior capsular structures of the shoulder in man. J Bone Joint Surg Br 50:858, 1968. 48. O’Brien SJ, Neeves MC, Arnoczky SN, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:451, 1990. 49. Fealy S, Dodeo SA, Dicarlo EF, O’Brien SJ: The developmental anatomy of the glenohumeral joint. J Shoulder Elbow Surg 9:217, 2000. 50. Ferrari DA: Capsular ligaments of the shoulder: Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20, 1990. 51. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208, 1981. 52. Bowen MK, Warren RF: Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 10:757, 1991. 53. Schwartz E, Warren RF, O’Brien SJ, et al: Posterior shoulder instability. Orthop Clin North Am 18:409, 1987. 54. Hurchler C, Wulker N, Mendilia M: The effect of negative intraarticular pressure and rotator cuff force on glenohumeral translation during simulated active elevation. Clin Biomech 15:306, 2000.
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55. Wulker N, Rossig S, Korell M, Thren K; Dynamic stability of the glenohumeral joint. A biomechanical study. Sportverletz Sportschaden 9:1, 1995. 56. Clark JM, Harryman DT 2nd: Tendons, ligamentous and capsule of the rotator cuff. J Bone Joint Surg Am 74:713, 1992. 57. Dugas JR, Campbell DA, Warren RF, et al: Anatomy and dimensions of rotator cuff insertions. J Shoulder Elbow Surg 11:98, 2002. 58. Curtis AS, Burbank KM, Tierney JJ, et al: The insertional footprint of the rotator cuff: An anatomic study. Arthroscopy 22:609, 2006. 59. Bassett R, Browne A, Morrey BF, et al: Glenohumeral muscle force and moment mechanics in a position of shoulder instability. J Biomech 23:405, 1990. 60. Miller SL, Gladstone JN, Cleeman E, et al: Anatomy of the posterior rotator interval: Implications for cuff mobilization. Clin Orthop Relat Res 408:152, 2003. 61. Comtet JJ, Herberg G, Naasan IA: Biomechanical basis of transfers for shoulder paralysis. Hand Clin 5:1, 1989. 62. deLuca CJ, Forrest WJ: Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomech 6:385, 1973. 63. Howell SM, Imobersteg AM, Seger DH, Marone PJ: Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am 68:398, 1986. 64. Lucas DB: Biomechanics of the shoulder joint. Arch Surg 107:425, 1973. 65. Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop 135:165, 1978. 66. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of the glenohumeral joint. Clin Orthop 173:3, 1983. 67. Brewer BJ: Aging of the rotator cuff. Am J Sports Med 7:102, 1979. 68. Hunt SA, Kwon YW, Zuckerman JD: The rotator interval: Anatomy, pathology, and strategies for treatment. J Am Acad Orthop Surg 15:4, 2007. 69. Jost B, Koch PP, Gerber C: Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg 9:336, 2000. 70. Nobuhara K, Ikeda H: Rotator interval lesion. Clin Orthop 223:44, 1987. 71. Fitzpatrick MJ, Powell SE, Tibone JE, Warren RF: The anatomy, pathology, and definitive treatment of rotator interval lesions: Current concepts. Arthroscopy 19:70, 2003. 72. Harryman DT, Sidles JA, Harris SL, Matsen FA: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53, 1992. 73. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop 244:172, 1989. 74. Kelly Am, Drakos MC, Fealy S, et al: Arthroscopic release of the long head of the biceps tendon: Functional outcome and clinical results. Am J Sports Med 33:208, 2005. 75. Walch G, Edwards TB, Boulahia A, et al: Arhtroscopic tentomy of the long head of the biceps in the treatment of rotator cuff tears: Clinical and radiographic results of 307 cases. J Shoulder Elbow Surg 14:238, 2005. 76. Boileau P, Baque F, Valerio L, et al: Isolated arthroscopic biceps tentomy or tendodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am 89:747, 2007.
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77. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1, 1944. 78. Lambert AE: A rare variation in the pectoralis minor muscle. Anat Rec 31:193, 1925. 79. Vare AM, Indurak GM: Some anomalous findings in the axillary muscles. J Anat Soc India 14:34, 1965. 80. Rothman RH, Marvel JP, Heppenstall RB: Anatomic considerations in the glenohumeral joint. Orthop Clin North Am 6:341, 1975. 81. Petersson CJ, Redlund-Johnell I: The subacromial space in normal shoulder radiographs. Acta Orthop Scand 55:57, 1984. 82. Weiner DS, MacNab I: Superior migration of the humeral head: A radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 52:524, 1970. 83. Flatow EL, Soslowsky LJ, Tcker JB, et al: Excursion of the rotator cuff under the acromion. Patterns of subacromial contact. Am J Sports Med 22:779, 1994. 84. Rathbun JB, MacNab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52:540, 1970. 85. Rothman RH, Parke WW: The vascular anatomy of the rotator cuff. Clin Orthop 41:176, 1965.
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Suggested Readings Hawkins RJ, Abrams JS: Impingement syndrome in the absence of rotator cuff tear (states 1 and 2). Orthop Clin North Am 18:373, 1987. Neer CS: Impingement lesions. Clin Orthop 173:70, 1983. Neviaser TJ: The role of the biceps tendon in the impingement syndrome. Orthop Clin North Am 18:383, 1987. Ovesen J, Nielsen S: Stability of the shoulder joint: Cadaver study of stabilizing structures. Acta Orthop Scand 56:149, 1985. Porterfield JA, DeRosa C: Musculature of the shoulder complex. In Porterfield JA, DeRosa C (eds): Mechanical Shoulder Disorders. Philadelphia, WB Saunders, 2004, p 47. Post M, Cohen J: Impingement syndrome: A review of late stage II and early stage III lesions. Clin Orthop 207:126, 1986. Watson MS: Classification of the painful arc syndromes. In Bayley JI, Kessel L (eds): Shoulder Surgery. New York, Springer-Verlag, 1982.
9/19/08 7:05:47 PM
CHAPTER 2 Clinical Biomechanics
of the Shoulder Complex Brian J. Eckenrode and Martin J. Kelley
PLANES OF MOTION
Shoulder function is the result of the complex interplay of the muscular, osseous, and supporting structures of the shoulder girdle. The lower extremity and trunk initiate and accumulate forces expressed at the shoulder and distal upper extremity. Ultimately, the shoulder positions the hand for precise movements necessary for activities of daily living and athletic performance.
Motion of the shoulder complex is described in relation to the cardinal planes—sagittal, coronal, and horizontal (Fig. 2-1). Shoulder flexion and extension occur in the sagittal plane, abduction and adduction in the coronal plane, and horizontal abduction and adduction in the horizontal plane. Internal and external rotation occur through the long axis of the humerus, affording a high degree of mobility in an infinite number of planes. This is typically assessed at 90 degrees of coronal plane abduction or with the arm at the side.
The articulations of the shoulder complex provide the shoulder with a range of motion that far exceeds that of any other joint. This movement is dependent on controlled and synchronous motion of all joints of the shoulder.1
The American Academy of Orthopaedic Surgeons (AAOS) no longer differentiates the plane of motion in which the arm is brought overhead; instead, they have adopted the term elevation.8 For the purposes of this chapter, shoulder elevation will be used to describe the flexion or abduction of the shoulder complex in the plane of the scapula or cardinal planes. Flexion and abduction will be specifically designated where applicable.
RESTING POSITION Ideally, the shoulder girdle musculature should be well balanced with respect to muscle strength and length to allow proper osseous orientation for optimal upper extremity function. Shoulder girdle suspension is reliant on the sternoclavicular ligaments,2 upper trapezius,3,4 levator scapulae, sternocleidomastoid, fascia,5 and atmospheric pressure.
Plane Of The Scapula In the resting position, the concave ventral surface of the scapula floats on the convex posterior thoracic wall, thus directing the glenoid fossa anteriorly approximately 30 to 45 degrees anterior to the coronal plane. This is referred to as the plane of the scapula (Fig. 2-2).11-13 The scapula has a slight anterior tilt in the sagittal plane,14 and the glenoid fossa exhibits a slight upward inclination in the resting position.15,16
The resting position of the shoulder girdle also depends on thoracic spine alignment and muscular linkages from the thoracic and cervical spine to the shoulder’s bony components.6,7 Shoulder girdle resting position is highly variable, depending on postural habits, hand dominance, occupation, muscle tone, and age.8 For example, the dominant shoulder of a competitive baseball pitcher tends to exhibit increased anterior tilt, depression, and abduction of the scapula compared with the nondominant side. The repetitive throwing cycle may result in abnormal and pathologic alterations. Burkhart and colleagues9 have described the asymmetrical malposition of the scapula in the throwing athletes as the SICK scapula (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement). Altered scapular position may produce scapular dyskinesis dynamically in the throwing cycle, affecting glenohumeral and acromioclavicular joint kinematics. This syndrome often manifests itself with pain and impaired throwing accuracy and velocity, along with altered scapular kinematics.10
Motion in the scapular plane is actually arm movement relative to the scapula as opposed to the trunk. This suggests that the plane of the scapula is not truly fixed, because the scapula translates forward during elevation.4 There are several unique biomechanical and anatomic features of scapular plane elevation:81 1. The joint surfaces have greater conformity.12,17 2. During elevation the inferior capsuloligamentous complex and rotator cuff tendons remain untwisted, because humeral rotation is not required (Fig. 2-3). 17
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THE ATHLETE’S SHOULDER Flexion Plane of scapula Horizontal adduction
Internal rotation Abduction
B
External rotation
Coronal abduction
Horizontal abduction
A
Extension
C
Figure 2-1. Motion of the shoulder complex. A, Planes of motion (superior view). B, Humeral external and internal rotation at 90 degrees of coronal plane abduction. C, Pure glenohumeral rotation at neutral and functional internal rotation. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 68.)
3. The supraspinatus and deltoid are optimally aligned for elevation. 4. Most functional activities are performed in this plane.18 These characteristics, specific to the scapular plane, can greatly enhance shoulder rehabilitation. By performing strengthening exercise in the plane of the scapula, rotator
cuff muscle strength can be optimized whereas unwanted passive tension on the rotator cuff tendons and capsuloligamentous complex (CLC) can be minimized. In the athlete with shoulder instability, the clinician can strengthen and perform range-of-motion exercises in the scapular plane, reducing potential anterior and posterior translation by eliminating stress on the deficient static restraints.
OSTEOKINEMATICS AND ARTHROKINEMATICS Scapulothoracic Joint
Figure 2-2. Scapular orientation in the plane of the scapula. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 65.)
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Scapulothoracic joint function enhances arm-trunk motion and glenohumeral stability as the scapula orients the glenoid to the humeral head. It also serves as a protective mechanism, because the joint and surrounding musculature absorb energy with a fall onto an outstretched arm.8 Kibler10 has described five distinct roles of the scapula: (1) it represents a stable part of the glenohumeral articulation; (2) allows for retraction and protraction along the thoracic wall; (3) elevates the acromion to decrease
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
A
19
B
Figure 2-3. Inferior view of the glenohumeral joint and capsuloligamentous complex. A, Scapular plane abduction. B, Coronal plane abduction. (From Johnston TB: The movements of the shoulder joint. A plea for the use of the “Plane of the Scapula” as the plane of reference in movements occurring at the humero-scapular joint. Br J Surg 25:252, 1937.)
impingement and coracoacromial arch compression in the throwing and serving motion; (4) serves as a base for muscle attachment; and (5) functions as a link in the proximal to distal sequencing of the kinetic chain. The failure of the scapula to perform these roles causes inefficient physiology and biomechanics, and therefore, inefficient shoulder function.10
Elevation and Depression Although gliding occurs between the scapula and thorax, the true fulcrum for motion is the sternoclavicular joint.8 Scapular elevation, movement of the scapula superiorly on the thorax (see Fig. 2-4),21 occurs primarily from activation of the upper trapezius4 and levator scapulae22; the rhomboid elevates with retraction.
The scapula is suspended on the axial skeleton by the sternoclavicular ligaments, indirectly through the clavicle,2 descending axioscapular muscles,3,5 coracoclavicular ligaments, atmospheric pressure,4 and fascia.5 Glenohumeral joint stability is maximized as the glenoid adjusts to support the humeral head.19 At rest, the scapula is positioned in the scapular plane. Scapular movement is primarily mediated by the oblique axioscapular muscles. The scapulothoracic joint is described with five degrees of freedom, three rotations and two translations (Fig. 2-4).20
Depression is movement of the scapula inferiorly on the thorax, and occurs in conjunction with scapular anterior or posterior tilting (see Fig. 2-4). Contraction of the pectoralis minor and serratus anterior causes depression and anterior tilting (protraction), whereas depression and posterior tilting are mediated by the lower trapezius.8 When a patient assumes the prone position, the shoulder girdle falls into a relatively elevated and protracted state. This is why muscle testing of the middle and lower trapezius requires manual setting of the scapula into an anatomic position.
Figure 2-4. Motions of the scapulothoracic joint. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 75.)
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THE ATHLETE’S SHOULDER
Abduction and Adduction Abduction is the movement of the medial border of the scapula away from the vertebral column (see Fig. 2-4).21 This motion is powered by the serratus anterior and pectoralis minor.3 The pectoralis major contributes to abduction by pulling on the fixed humerus, which then moves the scapula.8 Adduction is defined as movement of the medial border of the scapula toward the vertebral column (see Fig. 2-4).21 The rhomboids,22 middle trapezius,3 and lower trapezius23 are responsible for adduction.24 The levator scapulae are inactive unless elevation occurs. Posterior and Anterior Tilt Posterior and anterior tilt is scapular rotation about an oblique medial-lateral axis.25 Posterior tilt occurs as the acromion moves backward and anterior tilt occurs as the acromion moves forward (Fig. 2-5). Internal and External Rotation Internal and external rotation are described as scapular rotation about an oblique superior-inferior axis.25 External rotation can be visualized as the acromion moving posteriorly with the medial border of the scapula moving in an anterior direction; internal rotation can be visualized as the acromion moves anteriorly while the medial border moves posteriorly (see Fig. 2-5). Downward (Medial) and Upward (Lateral) Rotation Scapular downward and upward rotation occurs about an axis in the scapular body.25 Downward rotation is defined by rotation of both the glenoid downward and the inferior
Internal rotation
Anterior tilting
External rotation Posterior tilting
Upward rotation
Downward rotation Figure 2-5. Scapular variables of posterior tilt, upward rotation, and external rotation. (From Dayanidhi S, Orlin M, Kozin S, et al: Scapular kinematics during humeral elevation in adults and children. Clin Biomech (Bristol, Avon) 20:600-606, 2005.)
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angle of the scapula toward the spine (see Fig. 2-4). This is mediated by the rhomboids, levator scapulae, and pectoralis minor.4 Upward rotation is the rotation of the glenoid superiorly and movement of the inferior angle away from the spine. This motion is considered critical to shoulder performance. The scapula’s axis of rotation has been found to be slightly inferior to the scapular spine, approximately equidistant from the axillary and vertebral borders.26 A number of investigations have used three-dimensional techniques to quantify scapular movement relative to the thorax.27-32 McClure and associates31 have reported a mean ratio of glenohumeral to scapulothoracic motion of 1.7:1 in eight healthy shoulders in vivo using bone pin insertion directly into the scapula. During scapular plane elevation, the scapula was found to rotate upwardly (mean 50 degrees), rotate externally (mean 24 degrees), and tilt posteriorly (mean 30 degrees), whereas the clavicle elevated (mean 10 degrees) and retracted (mean 21 degrees). It was also found that scapular upward rotation and clavicular rotation occur approximately linearly throughout humeral elevation, especially beyond 50 degrees of elevation. Posterior tilting and external rotation motions were nonlinear, with the majority of these motions not occurring until after 90 degrees of arm elevation. Ebaugh and coworkers33 have reported that beyond 90 degrees elevation, the scapula moves into an anterior tilt, with external rotation motion having reached a plateau. These findings are similar to those of Ludewig, Lukasiewicz, Ebaugh, and their colleagues.29,30,33,34 Clinical assessment of scapular rotation during arm elevation should be examined as this is essential for normal shoulder function. The scapula should begin to migrate into lateral rotation by 60 degrees of elevation.8 If delayed, abnormal scapulohumeral rhythm may exist, possibly resulting in rotator cuff and bursa impingement because the glenoid and acromion have not begun their superior travel as the greater tuberosity approaches. Scapulohumeral Rhythm Proper scapular motion and stability are considered to be crucial to normal function of the shoulder31; therefore, scapulohumeral rhythm is an essential concept in the understanding of shoulder function. This phenomenon describes the relationship of motion between the scapula and humerus; however, the sternoclavicular and acromioclavicular joints also influence scapulohumeral rhythm. With active humeral elevation up to 30 degrees in the coronal or scapular abduction planes and up to 60 degrees of sagittal plane flexion, the scapula seeks a position of stability. This initial phase, called the setting phase, is variable and individualized.35 The scapula continues to rotate laterally around 60 degrees elevation,17 stabilizing against the thoracic wall with little superior or inferior migration. During
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
the first 90 degrees of motion, significant superior acromioclavicular joint migration occurs, corresponding to the clavicular elevation. At approximately 100 degrees of elevation, the coracoclavicular ligament begins to tighten, pulling on the posterior lip of the clavicle and producing clavicular upward rotation.36 The scapula continues to rotate, causing the center of rotation to shift toward the glenoid, resulting in medial and continued superior movement of the glenoid and lateral migration of the scapular inferior angle.16 Along with lateral rotation, the scapula orients the glenoid fossa anteriorly toward the sagittal plane.8 The scapula posteriorly tilts as the superior angle moves away from the thoracic wall with concomitant movement of the inferior angle toward the thoracic wall. Ten more degrees of acromioclavicular contribution occur after 135 degrees. In all, the scapula rotates approximately 60 degrees.3,14 Following the initial phase, the humerus and scapula maintain a particular relationship during arm elevation, described as a ratio of movement. This ratio has been investigated and quantified radiographically, goniometrically, and through the use of three-dimensional techniques. The classic work by Inman and colleagues35 has found a 2:1 ratio during both sagittal plane flexion and coronal plane abduction between 30 and 170 degrees of motion. Other studies have examined elevation of the glenohumeral joint in the scapular plane. Saha13 has reported a ratio of 2.3:1, similar to the findings by Inman and associates. Freedman and Munro15 have observed a 3:2 ratio from 0 to 135 degrees, with a decreased scapulothoracic contribution from 135 degrees to maximum elevation. Doody and coworkers14 have goniometrically determined a 1.74:1 ratio from 0 to 180 degrees, with varied inputs from the scapulothoracic and glenohumeral joints at different stages; the former contributes more during the middle phases of abduction (90 to 140 degrees). Poppen and Walker16 have discovered a 4.3:1 ratio from 0 to 30 degrees, followed by a 1.25:1 or 5:4 ratio from 30 to 180 degrees of elevation. McClure and colleagues31 have reported a mean ratio of glenohumeral-to-scapulothoracic motion of 1.7:1 in eight healthy shoulders in vivo using bone pin insertion directly into the scapula. McQuade and Smidt32 have demonstrated that during dynamic humeral elevation, the scapulohumeral rhythm changes, depending on the phase of elevation and amount of external load on the arm. For unloaded elevation, the scapulohumeral rhythm ranges from 7.9:1 to 2.9:1, for light load elevation, 3.1:1 to 4.3:1; and for heavy load elevation, 1.9:1 to 4.5:1. Graichen and associates37 have noted a ratio of 1.5:1 at 60 degrees to 2.4:1 at 120 degrees for passive scapular plane abduction, using open magnetic resonance imaging and three-dimensional image processing. Passive elevation follows a pattern similar to that of active elevation, except that the scapula tends to move into a position
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21
of internal rotation,33 with less upward rotation early and more upward rotation in the last two phases.32 Borstad and Ludewig27 have examined the effect of eccentric versus concentric control on three-dimensional scapular kinematics. They found a decrease in scapular anterior tilt and increase in scapular internal rotation during the eccentric phase of arm elevation at 80, 100, and 120 degrees. No significant difference was noted in scapular position with eccentric and concentric trials for any scapular variable below 80 degrees. Overhead shoulder function, especially eccentric lowering, may alter scapular kinematics and predispose athletes to injury. Throwing athletes demonstrate increased scapular upward rotation, internal rotation, and retraction.38 This adaptation may allow for clearance of the subacromial space and improve throwing performance. The results for scapulohumeral rhythm vary somewhat because of the type of measurement technique used (Table 2-1). However, the relationship between glenohumeral and scapulothoracic motion is critical and is generally considered to be 2:1, culminating in 120 and 60 degrees, respectively. Caution is required when comparing passive and active glenohumeral-to-scapulothoracic ratios and their phases of contribution.8 During passive motion, the muscles that drive the scapula are inactive; thus, initiation of scapular movement will lag compared with active motion, being dependent on the glenohumeral capsuloligamentous structure’s elasticity and expansion. This explains why during passive movement, scapular motion may not be detected until 70 to 90 degrees. Viewed another way, scapular upward rotation is partly related to tension developed in the CLC during elevation. Patients with hyperelastic tissue or instability probably demonstrate less upward scapular rotation during active elevation because there is more “play” in the CLC. The scapula will move earlier with
TABLE 2-1 Comparison of Ratios of Active Glenohumeral to Scapulothoracic Rhythm in the Plane of Scapula Study, Year
Ratio ( Average)
Inman et al, 194435
2:1
Saha, 1961
13
2.3:1
Freedman and Munro, 196615 3:2 Doody et al, 197014
1.74:1
Poppen and Walker, 1976 McClure et al, 2001
16
31
Graichen et al, 2000
1.7:1
37
McQuade and Smidt, 1998
1.25:1 or 5:4 1.5:1 to 2.4:1
32
7.9:1 to 2.1:1 (passive range of motion); 1.9:1 to 4.5:1 (with load)
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THE ATHLETE’S SHOULDER
movement of the humerus if adhesions exist in the capsuloligamentous complex. Therefore, passive rather than active assessment of scapulohumeral rhythm tends to be more sensitive in determining restrictions of the capsuloligamentous complex. Effect of Shoulder Pathology on Shoulder Rhythm. Quantitative scapular kinematics studies have shown abnormal scapular motion associated with certain pathologies.39,40 Unfortunately, the equipment used to attain these measurements is not clinically applicable. The clinician is left with visual inspection and linear measurements that have low reliability.41 Active movement assessment of the shoulder complex is necessary to determine whether a dysfunctional scapulohumeral rhythm exists, because this is often associated with muscular weakness or abnormal activation patterns.8 Dramatic or subtle scapular dyskinesia may be visualized on active arm elevation in the sagittal plane, possibly indicating a nerve palsy, instability, or motor dyskinesia (Fig. 2-6). Weakness of the rotator cuff muscles typically results in compensation by the patient shrugging or excessive scapular elevation. Pain or contracture of the glenohumeral capsuloligamentous complex will manifest during active arm motion by increased scapular elevation and lateral rotation. Shoulder pathology has been demonstrated to have an adverse effect on scapulothoracic rhythm. Paletta and coworkers,39 using a two-plane radiograph series, found that
subjects with shoulder instability and subjects with a rotator cuff tear demonstrate altered glenohumeral-scapulothoracic motion relationships. Mell and colleagues42 have reported that shoulder kinematics are altered in subjects with a rotator cuff tear. The scapula was found to elevate more for the same amount of humeral elevation than in normal shoulders or shoulders with tendonopathy. The presence of this kinematic alteration in cuff tear patients and not in tendinosis patients suggests that it is related to loss of cuff strength and function rather than pain. In shoulders with known instability, Von Eisenhart-Rothe and colleagues43 have demonstrated an increase in scapular internal rotation in the transverse plane and a malcentering of the humeral head in the direction of the instability. Their study suggested that scapular positioning is relevant for humeral head decentering and should be considered in the treatment of different forms of atraumatic shoulder instability. Lukasiewicz and associates30 have reported that subjects with impingement syndrome demonstrate significantly less posterior tilt, greater superior translation at the horizontal, and maximal elevation when compared with nonimpaired individuals. Ludewig and Cook34 have demonstrated decreased posterior tilt, external rotation, and upward rotation in subjects with impingement. The presence of posterior tilting may be important functionally to allow for clearance of the humeral head and rotator cuff tendons under the anterior aspect of the acromion during elevation.31 Limited scapular posterior tilt could result from a shortened pectoralis minor, restricted scapular mobility, and inadequate shoulder complex muscle activity. Altered kinematics may result as patients tend to rotate the scapula to a greater degree to avoid impingement and reduce the requirement for elevation at the glenohumeral joint.42 Effect of Posture on Shoulder Rhythm. Scapulohumeral rhythm and strength may also be influenced by postural changes and adaptively shortened muscular structures. Increased thoracic kyphosis may lead to a decrease in posterior tilt and lateral scapular rotation with humeral elevation.44 Smith and coworkers45 have found a reduction in isometric shoulder strength in protracted and retracted scapular positions when compared with neutral, suggesting compromised shoulder muscle function and deviation from normal resting scapular position.
Figure 2-6. Patient with a long thoracic nerve palsy. Note the prominence of the medial border of the scapula, with active elevation of the right shoulder.
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During active arm elevation, the pectoralis minor becomes passively lengthened by scapular upward rotation, external rotation, and posterior tilting.31,34 Individuals with a shortened pectoralis minor exhibited decreased scapular upward rotation, external rotation, and posterior tilting during elevation.46 The finding of a short pectoralis minor muscle suggests an increased risk for impingement in this
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
23
population and may contribute to altered mechanics in throwers.9 Deviating patterns of external rotation or the inability to rotate the humerus externally change the scapulohumeral rhythm substantially.47 Anterior tightening procedures, such as the Putti-Platt or Magnuson-Stack procedure or a tight Bankart repair, are likely to result in a loss of external rotation and elevation.48 Athletes with limited external rotation range of motion tend to exhibit an altered scapulohumeral rhythm, which may affect throwing performance and overhead function. Excessive restriction of external rotation caused by an overtightened anterior-inferior CLC increases posterior translation, exacerbating wear on the posterior glenoid and ultimately leading to the long-term complication of secondary osteoarthritis.48-50
Sternoclavicular Joint The sternoclavicular joint represents the single bony articulation between the axial skeleton and upper extremity. This is a monumental responsibility, particularly because the amount of articular contact is the least of all the major joints in the body.51 The sternoclavicular joint serves as the pivot point for scapular elevation-depression and abduction-adduction. Clavicular elevation and depression occur through an axis in the sagittal plane. The sternoclavicular joint is reported to allow for 45 to 60 degrees of elevation and 5 degrees of depression.14,52 Elevation is limited by tension on the costoclavicular ligament.2,4,51,53,54 Depression of the sternoclavicular joint is limited by the superior joint capsule and interclavicular ligament, and contact between the clavicle and first rib.21 Although only 5 degrees of active depression is available, greater excursion results, particularly when the clavicular suspensory muscles are lacking. Clavicular protraction and retraction occur through an axis in the transverse plane,4 allowing approximately 15 degrees of motion in each direction.52 Because the axis is oblique, retraction is accompanied by elevation and protraction is combined with depression.2 Protraction is limited by the posterior fibers of the costoclavicular ligament, posterior sternoclavicular capsule, and posterior fibers of the interclavicular ligament.51,55 Retraction is restricted by the anterior costoclavicular fibers and anterior sternoclavicular capsule (Fig. 2-7). Rotation occurs through the longitudinal axis of the clavicle. During flexion and abduction, Inman and colleagues35 have demonstrated approximately 40 degrees of upward rotation, as defined by the direction of the anterior edge of the clavicle. The upward rotation motion begins at approximately 90 degrees of elevation, and becomes increasingly greater at the end range. Tension of the coracoclavicular ligaments regulates this upward rotation. As the scapula moves into elevation, the base of the coracoid process, which
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A
B
C
D
Figure 2-7. Sternoclavicular motion through two axes. Illustrated are depression (A) and elevation (B) through the sagittal axis, and retraction (C) and protraction (D) through the superomedial to inferolateral oblique axis. (From Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49-70, 1965.)
is the insertion of the coracoclavicular ligaments, begins to move distally. This produces a downward pull on the posterior clavicle, thus causing upward rotation. Approximately 10 degrees of downward rotation are available. Even with trauma to the sternoclavicular joint, close to normal range of motion and full function are achieved, but pain acts as the limiting factor. In patients with hypomobility of this joint, shoulder elevation may be limited to 100 degrees, with abduction and internal rotation the most painful movements.
Acromioclavicular Joint The acromioclavicular joint is a plane-type joint formed by the articulation of the distal clavicle with the acromion of the scapula. Three degrees of freedom are available at the acromioclavicular joint; however, they rarely occur individually.52 Motion occurs in a vertical, anterior-posterior, and medial-lateral direction (Fig. 2-8). The vertical axis allows the scapular vertebral border to “wing” and the glenoid fossa to face anteriorly.51,52 The acromion glides forward and backward as the scapula’s medial border swings away from and into the thorax— scapular internal and external rotation. This motion is checked by tension in the conoid and trapezoid ligaments. Motion about the anteroposterior axis results in enlarging or shrinking the angle formed by the clavicle and spine of the scapula in the frontal plane.21 This axis allows for scapular abduction and adduction, as described by Mosley.52 An axis through the coronal plane permits anterior tilting of the superior angle, causing the inferior angle
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THE ATHLETE’S SHOULDER Vertical axis
Winging of vertebral border (50° max.)
Sagittal (anteroposterior) axis
A
Inman and coworkers35 have warned against screw fixation negating acromioclavicular joint motion. Several investigators have found screw fixation or coracoclavicular ossification to have little or no effect on shoulder elevation.58,59 In fact, when Kirschner wires were attached to the clavicle of a patient whose distal clavicle was fixated to the coracoid by a screw, full clavicular rotation was observed.60 Kennedy and Cameron58 have reported that patients older than 50 years have less satisfactory results and painful end range abduction with screw fixation. It was concluded that this group relies more on the coracoclavicular ligamentous play than younger patients.
Glenohumeral Joint
Frontal axis
B
C Figure 2-8. Three axes of motion shown through the acromioclavicular joint. A, Vertical axis allows the glenoid to face toward the sagittal or coronal plane. B, Sagittal axis allows slight medial and lateral rotation. C, Coronal axis allows anterior and posterior tilting. (From Moseley HF: The clavicle: Its anatomy and function. Clin Orthop 58:17-27, 1958.)
to lift posteriorly. Anterior tilting is restricted by the anterior acromioclavicular and trapezoid ligaments, whereas posterior tilting is restricted by the thorax and posterior acromioclavicular and conoid ligaments.51 Inman and associates35 have demonstrated that approximately 10 degrees of motion occur at the acromioclavicular joint during the first 30 degrees of flexion and abduction, and then again in the last 45 degrees of motion. The acromioclavicular joint contributes greater motion at the end range of elevation,3 although total motion is restricted to about 5 to 8 degrees per axis.56 When irritation of this joint exists, clinical findings reveal pain at all shoulder end ranges, particularly during horizontal adduction. The acromioclavicular joint may compensate for lost motion in the presence of glenohumeral joint restriction.57
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The glenohumeral joint is a classic ball-and-socket joint between the humeral head and glenoid fossa of the scapula, and is the most mobile joint in the body.1,21,61 This high level of mobility challenges the inherent stability, as evidenced by the articulation between the larger convex humeral head and shallow concave glenoid fossa. This joint is an intricate complex with a sometimes fragile system of checks and balances; its vulnerability is demonstrated by the number of patients seen with pathology of associated static and dynamic components. The glenohumeral joint has three axes of motion along the cardinal planes of the body: sagittal, frontal, and horizontal. Sagittal plane flexion and frontal plane abduction require concomitant humeral rotation. The humerus externally rotates with abduction11,12,4,,62 and internally rotates with flexion.23,63,64 With scapular plane elevation, no external rotation is required.14 Only 25% to 30% of the humeral head is covered by the glenoid surface in any given anatomic position.11 The average humeral head diameter is 44 mm compared with a glenoid diameter of 25 mm. The fossa is deepened by a 2-mm ridge of labral fibrocartilage tissue.65 Although the bony surfaces of the humeral head and glenoid fossa have slightly different curvatures, their cartilaginous articular surfaces have approximately the same radius of curvature.21,66-68 The radius of curvature quantifies the amount of curve in a surface by describing the radius of the circle from which the surface is derived. These surfaces have similar curvatures; thus, there is a high degree of congruence, which helps disperse loads across a larger surface area, reducing articular surface stress. The concept of glenohumeral motion occurring with a certain degree of rotation (spin), roll, and glide is well accepted (Fig. 2-9). MacConnail and Basmajian64 have developed the term roll-gliding to describe joint motion between incongruent, concave, and convex surfaces. The direction of rolling and gliding components is dependent on whether the concave or convex surface is moving. The convex-concave theory of arthrokinematics dictates that if a convex surface
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
initial phase, the humerus center of rotation remains constant, moving 1 to 2 mm upward or downward relative to the glenoid center. It was concluded that after the initial rise, the humeral head will rotate or spin on a more or less fixed center, with little if any excursion. Harryman and associates72,73 have reported an average superior migration of 0.7 mm during abduction and 0.8 mm during flexion. A
B
Using a three-dimensional technique of stereophotogrammetry on cadaver shoulders, Kelkar and coworkers74 have found an average vertical excursion of 1.29 mm occurring through an arc of 180 degrees of scapular plane abduction and an average of 0.94 mm of superior glide in the first 30 degrees of motion (Fig. 2-10). In support of Poppen and Walker’s findings,16 they concluded that the initial superior rise occurs because of the dependent (inferior) state of the humerus when unloaded but after 30 degrees, pure glenohumeral joint rotation occurs. Yamaguchi and colleagues75 have demonstrated a progressive superior translation of the humeral head on the glenoid, with increasing arm elevation in patients with symptomatic and asymptomatic rotator cuff tears. The symptomatic and asymptomatic rotator cuff tear groups exhibit an increase in superior head migration from 30 to 150 degrees during scapular plane elevation, as well as a disruption of normal glenohumeral kinematics. However, shoulder pain is not always present with the superior migration.
C
moves on a concave surface, then gliding occurs in the opposite direction to the rolling; if a concave surface moves on a convex surface, then rolling and gliding occur in the same direction. The more congruent the surfaces, the more gliding occurs and the more incongruent, the more rolling takes place.69 The disproportion between the glenohumeral articular surfaces would then dictate that rolling dominates. In other investigations, however, these findings were not validated. There has been much debate regarding the translatory motion of the glenohumeral joint. Calliet6 and Saha13,70 have stated that humeral head rolling on the glenoid is the predominant motion and that this is accompanied by some amount of gliding. Perry5 has stated that gliding is the primary component motion and that rolling is not significant to glenohumeral motion, other than the first 3 mm of superior excursion. Howell and colleagues71 have noted that rotation is the dominant movement, with gliding as the initial movement. Poppen and Walker16 have radiographically determined the initial 30 degrees of scapular plane elevation; often, from 30 to 60 degrees, the humeral head glides upward on the glenoid fossa approximately 3 mm. After this
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It is important for the clinician to realize that the humeral head does not truly“depress”with elevation, and that gliding is both superior and inferior.8 The humeral head center of rotation remains relatively constant with the center of the glenoid. What changes, through rotation and subtle gliding of 1 to 2 mm (roll-glide), is the humeral articular contact point moving inferiorly to superiorly on the humeral head.16,74,76 The greater tubercle “depressing”
1
0 Translation (mm)
Figure 2-9. Three types of articular movement occur at the glenohumeral joint. A, Rotation. B, Rolling. C, Gliding. (From Matzen FA III, Zuckerman J: Biomechanics of the shoulder. In Frankel VH, Mordin M [eds]: Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989, p 231.)
–1
–2
–3 0
30
60
90
120
150
180
Arm elevation (degrees) Figure 2-10. Normal superior glide during plane of the scapula abduction. (From Kelkar R, Flatow E, Bigliani L, et al: A stereophotogrammetric method to determine the kinematics of the glenohumeral joint. Adv Bioeng 19:143, 1992.)
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(as the humerus elevates) during palpation must not be mistaken for a sign of humeral head inferior gliding. Instead, greater tubercle movement represents medial migration beneath the acromion. Controversy also exists regarding the translation or gliding of the humeral head in the anterior and posterior directions. Howell and associates71 have radiographically evaluated anterior and posterior translation with the arm positioned in varying degrees of horizontal adduction/abduction and rotation (Fig. 2-11). It was concluded that the humeral head normally translates 4 mm posteriorly in 90 degrees of abduction, full external rotation, and maximal horizontal abduction, but subjects with known anterior instability demonstrate anterior, not posterior, translation in the same position. Harryman and coworkers73 have performed a biomechanical analysis on cadavers using telemetry; they found approximately 3.8 mm of anterior translation with flexion and 5 mm of posterior translation with extension. With tightening of the posterior capsule, there is a significant increase in anterior translation and, to some extent, superior humeral head translation. Additionally, it was noted that external rotation and internal rotation, performed with the humerus at the side, produces posterior and anterior gliding, respectively. Werner and colleagues77 have examined the effects of capsular tightening on humeral head translation in cadavers. The capsular plication causes a translation directed away from the plication site. Moore and associates78 have studied the kinematics of glenohumeral joint translation, with varying degrees of internal and external rotation at 90 degrees abduction. With increasing external rotation, anterior translation decreases and the humeral head moves in the posterior direction.
–4 mm extension (ext. rot.)
Figure 2-11. Axillary view (inferior through the glenohumeral joint) in 90 degrees of abduction, full external rotation, and horizontal abduction. The geometric center of the humeral head is 4 mm posterior to the center of the glenoid fossa, demonstrating normal posterior, not anterior, translation. ext. rot., external rotation. (From Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232,1988.)
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These studies have concluded that the direction of translation is dictated by tightening of the capsuloligamentous complex opposite the side of translation (Fig. 2-12). Shoulder movement causes the static restraints to become taut; they not only serve to counteract but to reverse humeral head movement. If the static restraints are stretched or their attachments compromised, abnormal translation occurs.8 For example, in the presence of a Bankart lesion or loose anterior and inferior capsule, the humeral head would translate anteriorly when placed in abduction and external rotation, as opposed to posteriorly. In summary, an initial superior glide occurs with elevation, not inferior, until the head centers and rotation occurs. During shoulder extension and external rotation, the humeral head glides posteriorly and, with shoulder flexion and internal rotation, the humeral head glides anteriorly.21,67,73,79-81 This is likely because of the constraints of the capsular tissue and glenohumeral ligaments. These findings contradict the traditionally taught kinematics—the concave-convex rule.21 Performing joint glides to re-establish proper joint mechanics based on the traditionally accepted idea of joint motions is questionable. Joint mobilization is essential for relieving pain, producing muscular relaxation, and increasing joint range of motion. These techniques are effective because directional mobilizations “stretch” isolated portions of the capsuloligamentous complex. By improving capsuloligamentous pliability in any direction, regardless of the directions in which the humeral head translates during motion, proper joint mechanics and range of motion are restored in all ranges of motion and planes.8
STABILITY Stability of the glenohumeral joint is provided by the articulating surfaces, capsular and ligamentous structures, and synchronous activity of the rotator cuff, biceps, deltoid, and scapular muscles.82 Stability or instability research has been based primarily on cadaveric and operative investigations. Focus has been on anterior instability because this is most commonly seen, followed by posterior instability and inferior instability. Four structures are considered to be the main factors in stability of the shoulder—articular surfaces, labrum, capsuloligamentous complex, and rotator cuff. Scapular muscle function will be discussed separately. Related factors will also be addressed in this section.
Articular Surfaces The glenohumeral articular surfaces have been shown to provide static stability to the joint.83 The surface of the glenoid fossa has been found to be one third to one quarter that of the humeral head,70,84-87 and this difference in the size of the articular surfaces allows a large degree of
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27
Superior (90° sup) 10 mm
5 Abd Flex Posterior (180°)
Anterior (0°) 10 mm
5
ER 0
ER 90 ER 45
5
10 mm
IR 0
IR 90
IR 45
5
10 mm Inferior (90° inf) Translation
SD
Direction
Abd
3.8 mm
2.2 mm
83° sup
Flex
7.3 mm
3.2 mm
18° sup
ER 0
0.9 mm
0.4 mm
19° inf
ER 45
4.3 mm
2.3 mm
145° inf
ER 90
5.6 mm
1.8 mm
160° inf
IR 0
6.1 mm
4.0 mm
22° inf
IR 45
8.0 mm
3.9 mm
16° inf
IR 90
12.0 mm
8.2 mm
5° inf
Figure 2-12. Translation at the end of several movements with intact capsule. The values indicated are mean translations in the actual directions (directions are defined relative to a strictly anterior direction: 0 degrees, posterior direction; 180 degrees, superior and inferior parts, respectively). Abd, abduction; Flex, flexion; ER 0, external rotation at 0 degrees of abduction; ER 45, external rotation at 45 degrees of abduction; ER 90, external rotation at 90 degrees of abduction; IR 0, internal rotation at 0 degrees of abduction; IR 45, internal rotation at 45 degrees of abduction; IR 90, internal rotation at 90 degrees of abduction. (From Werner CM, Nyffeler RW, Jacob HA, Gerber C: The effect of capsular tightening on humeral head translations. J Orthop Res 22:194-201, 2004.)
mobility. Saha,36 using cadaveric radiographic studies, has determined that the normal glenoid is retroverted approximately 7.4 degrees, serving to discourage anterior humeral translation. Of 21 shoulders with anterior instability, 80% demonstrated 2 to 10 degrees of glenoid anteversion. A corresponding increase in humeral retroversion was believed to predispose the joint to anterior instability. Basmajian and Bazant57 have discovered that a 5-degree superior tilt of the glenoid assists in preventing inferior humeral migration.
resulting in a misleadingly flat glenoid shape on radiographs.88
Congruence can be defined as the difference in the radii of the humeral head and glenoid articulating surfaces.82 The closer this difference is to zero, the more congruent is the joint. Soslowsky and coworkers83 have demonstrated excellent congruency between the glenoid and humeral head using three-dimensional stereophotogrammetry to quantify the articular geometry in 32 cadavers. They found an average ratio of the radii of curvature between the two surfaces of 0.99 ⫾ 0.05. This conformity of surfaces dictates that pure rotation with minimal translation occurs at this joint.74 The articulating cartilage surfaces are much more conforming than the underlying bone surfaces,
The glenoid labrum is a wedge-shaped ring of fibrocartilage that encircles the bony glenoid, deepening the glenoid cavity and serving to bridge bone to the glenohumeral ligaments and biceps tendon (Fig 2-13). Using cadavers, Howell and Galinet65 have found the average depth of the socket and labrum to be 9 mm superiorly-inferiorly and 5 mm anteriorly-posteriorly. The labrum was found to contribute approximately 50% of the total depth of the socket, and detachment of the labrum anteriorly, as in a Bankart lesion, may reduce the depth of the socket in the anterior-posterior direction. Regional variation in the labrum exists; the inferior portion is immobile and firmly
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A built-in safeguard promoting articular stability, often forgotten, is the effect of scapular motion.8 Scapular mobility allows the glenoid to adjust, providing a stable osseous platform for the humeral head.89 This movable base may compensate for articular deficiencies.
Labrum
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produce anterior glenohumeral dislocation clinically requires inferior glenohumeral ligament plastic deformation in addition to the Bankart lesion. Resection of the glenoid labrum has been reported to reduce the effectiveness of compression-stabilization by approximately 10% to 20%.95 Chondral-labral defects reduce the height of the glenoid, which in turn significantly reduces the stability ratio.96 Compression by muscle activity and capsuloligamentous tightening increases the stability of the labrum.94 Rodosky and associates,97 using dynamic cadaveric shoulder models, have created superior labral lesions and found that these shoulders show a decreased ability to resist external rotation when abducted and internally rotated. Superior labral defects have been found to decrease torsional rigidity and increase inferior glenohumeral ligament strain, which contributes to anterior instability.88
Capsuloligamentous Complex
Figure 2-13. Labral insertion to the glenoid rim. (From O’Brien SJ, Arnoczky SP, Warren RF, Rozbruch RA: Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, p 14.)
attached to the glenoid and the superior portion is attached more loosely, allowing for substantial range of motion of the glenohumeral joint.88 The labrum is the weak link (younger than 30 years) when a continuous progressive low load is exerted across the anterior capsular mechanism.90 Hara and colleagues91 have reported that the anterior-inferior portion of the labrum is relatively weak, consistent with clinical findings of lesions commonly identified in anterior shoulder dislocation. Bankart,92 Rowe,93 and Rowe and Sakellarides,19 proponents of labral stability influence, have emphasized the importance of the labrum linking the capsule to the glenoid bony rim as opposed to a buttress effect, in which the labrum acts as a physical block to humeral head displacement. Recurrent instability tends to erode the articular cartilage of the anterior inferior glenoid rim and decreases concavity.88 With the labrum intact, the humeral head resists tangential forces as much as 60% of the compressive load.94 The amount of humeral head translation needed to
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The glenohumeral joint capsule provides passive stability at the extremes of glenohumeral motion.77 The capsule does not only limit rotation and prevent excessive translations, but also causes a coaptation and obligate translation of the humeral head on the glenoid at the end of passive movements. The glenohumeral ligaments and coracohumeral ligaments reinforce the capsule and serve as static restraints (Fig. 2-14).98-104 Ligaments attach bone to bone and act to guide and limit motion, with their constraining function evident as these structures become taut. Essentially, ligaments fulfill a dual stabilizing role—to provide a barrier against translation103 and to increase articular compressive forces as they tighten.51 The extreme of this is seen in the presence of capsular adhesions. In the presence of fibrotic capsuloligamentous tissue, glenohumeral articular compression can be so oppressive that normal rotation is obliterated.8 The role of any specific component of the stabilizing system varies with glenohumeral joint position and direction of the opposing force.88 A functional interplay or interdependence exists between anterior and posterior and superior and inferior components of the capsuloligamentous system. This circle concept of capsuloligamentous stability implies that excessive translation in one direction may damage the restraints on both the same and opposite sides of the joint.105 The capsule is a continuous structure; injury or repair to one region of the capsule may have an adverse effect on the properties of the neighboring regions and on joint function.106 Coracohumeral Ligament The coracohumeral ligament (CHL) is intimately related to the rotator cuff and actually reinforces the supraspinatus superiorly and inferiorly.107 The CHL and superior glenohumeral ligament join to make up the rotator cuff interval, which bridges the supraspinatus and subscapularis
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Figure 2-14. Lateral view of the glenoid showing the capsuloligamentous complex attachments in relation to the deep muscles and tendons. (From Turkel SJ, Panio MW, Marshal JL: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981.)
(Fig. 2-15).23,73 The rotator cuff interval is the primary restraint against inferior and posterior translation of the adducted shoulder. Sectioning the interval increases anterior and posterior translation, whereas imbricating it significantly reduces translation in both directions. Harryman and coworkers73 have found that tightening the rotator cuff interval leads to an 8-degree loss of flexion and an 18-degree loss of extension. This is consistent with the study by Terry and colleagues,102 who found the CHL to be a primary restraint in flexion and extension. Harryman and associates73 have also found external rotation performed with the arm adducted decreased by 38 degrees and adduction by 8 degrees when the interval was imbricated. Gerber and coworkers,108 using cadavers, have found that Supraspinatus
closure of the rotator interval limits external rotation of the adducted arm by a mean of 30.1 degrees (56.4% of normal), whereas it had no significant effect on external rotation of the abducted arm. In addition to preventing inferior instability with the arm at the side, the CHL restricts external rotation and extension.72,85,100,102,109 The significance of the coracohumeral ligament is not only important in stability but in the presence of supraspinatus pathology. Because the CHL limits external rotation when the arm is adducted, exercising into excessive external rotation while the arm is adducted should be approached with caution. The passive tension developed in the CHL translates directly to the compromised supraspinatus,
CHL Coracoid
Coracoid
Supraspinatus RI capsule
Biceps SGHL
Subscapularis
A
Biceps in intertubercular groove
B
Subscapularis
Figure 2-15. Schematic of the rotator cuff interval. A, Anterior view. B, Cross-sectional lateral view. CHL, coracohumeral ligament; RI, rotator interval; SGHL, superior glenohumeral ligament. (From Fitzpatrick MJ, Powell SE, Tibone JE, Warren RF: The anatomy, pathology, and definitive treatment of rotator interval lesions: Current concepts. Arthroscopy 19:70-79, 2003.)
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THE ATHLETE’S SHOULDER
causing pain or further disruption.8 Additionally, release of the interval and subsequent suturing during a rotator cuff repair need to be respected by limiting postoperative external rotation motion when the arm is at the side. Superior Glenohumeral Ligament The superior glenohumeral ligament (SGHL) prevents inferior displacement of the humeral head,84,110 limits external rotation at 0 degrees of rotation,100,102,104 and acts as a restraint during extension. A lesion of the rotator cuff interval, which is associated with anterior and inferior instability of the glenohumeral joint,111 may be caused by a deficiency in the superior glenohumeral ligament. The SGHL and anterior band of the coracohumeral ligament also serve as restraints up to 50 degrees abduction and external rotation.112 Both ligaments have been implicated as the source of fatigue pain when a mild downward load is placed on the arm.113 Following shoulder surgery, and in the presence of reflex inhibition, tension that develops in these ligaments may partly explain postoperative pain.8 Once these ligaments have stretched, as in hemiplegia, it is difficult to regain stability.57 Middle Glenohumeral Ligament Turkel and associates104 have investigated the stabilizing mechanisms of the glenohumeral joint that prevent anterior dislocation by sequentially incising the glenohumeral anterior and posterior soft tissue structures. The subscapularis was initially cut, followed by the SGHL, middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament (IGHL). It was found that anterior dislocation occurs at neutral when externally rotated, with the subscapularis muscle providing primary stability. At 45 degrees of abduction, primary stability is provided by the subscapularis, MGHL, and anterosuperior fibers of the IGHL. Approaching 90 degrees of abduction, the inferior glenohumeral ligament prevents dislocation during external rotation. At 90 degrees of abduction and full external rotation, the joint remains stable, until the posterior cuff was cut, which resulted in anterior dislocation. This study104 was performed with scapular fixation while abducting the humerus to 90 degrees, which does not take into consideration scapular rotation; 90 degrees in this investigation corresponds to approximately 120 to 135 degrees of true shoulder elevation.8 A limitation of this study was that it did not introduce horizontal abduction or apply any anterior force. Gerber and coworkers108 have studied the effect of capsular contractures on the passive range of movement of the glenohumeral joint. Their data suggest that anterior plications restrict external rotation, whereas posterior plications restrict internal rotation. Plications of the superior aspect of the capsule are largely responsible for restrictions of motion with the arm in an adducted position. Conversely, plications of the inferior aspect of the capsule have more influence on motion of the abducted arm. The results of this study have demonstrated that contracture of the
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posterosuperior aspect of the capsule may limit internal rotation and flexion, whereas contracture of the anteroinferior aspect of the capsule, including the anteroinferior glenohumeral ligament complex, increasingly limits motion with increasing abduction of the arm. Contracture of the posterior aspect of the capsule plays an important role in limiting internal rotation, flexion, and abduction, even without inferior plication. The MGHL was found to have stabilizing effects at 0 and 45 degrees of abduction.8 External rotation at these positions causes tightening of the MGHL, providing a barrier against anterior displacement.104,114 Turkel and colleagues104 have reported that this ligament is loose at 90 degrees of abduction and full external rotation. Other investigations have shown that the MGHL, along with the SGHL, is similar to the IGHL in regard to abduction and external rotation,100,115 and that the MGHL is found to tighten during flexion combined with external rotation.102 The MGHL also functions to support the arm and provide anterosuperior stability.112 Inferior Glenohumeral Ligament The IGHL is the thickest of the glenohumeral ligaments, with an anterior band, posterior band, and axillary pouch. As with the other glenohumeral ligaments, the IGHL’s ability to restrict motion depends on humeral elevation and rotation. At 0 degrees abduction, the anterior band becomes the primary stabilizer,112 tightening when the humerus is externally rotated at neutral and when the humerus is abducted without external rotation.102 When external rotation is performed at 90 degrees of abduction, the entire IGHL tightens while the superior or anterior band wraps snugly across the humeral head, checking anterior displacement.99,102,104,114,116 O’Connell and colleagues100 have found the greatest amount of strain through the IGHL at 90 degrees of abduction and full external rotation. Kuhn and associates117 have suggested that the inferior glenohumeral ligament is the most important restraint to external rotation in both the neutral and abducted positions. The clinical implication is that external rotation may contribute to failure of the inferior glenohumeral ligament in patients with shoulder instability. The IGHL has the ability to stretch considerably before ligament failure, suggesting that lateral translation of the humeral head is possible under loads that would allow the head to override the glenoid rim.88,118 This supports the clinical finding that certain patients can sublux without disruption of the capsule or its insertion sites. Repetitive loading of the inferior glenohumeral ligament at increasing levels of subfailure strain shows a dramatic increase in peak force with elongation, suggesting that the capsule may be subject to plastic deformation, especially after trauma.101,119 The IGHL appears to be a single identifiable complex that stabilizes against abnormal anterior and posterior humeral
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
31
head translation, becoming taut with external and internal rotation, respectively, during arm elevation.99 Conversely, it can be appreciated how adhesions or contracture of this structure could limit external rotation, internal rotation, and elevation.
internally rotated in the abducted position.8 The posterior rotator cuff and capsule are the primary restraints against posterior instability; the anterior capsuloligamentous complex assists with posterior stability and the posterior structure assists with anterior stability.102
Internal rotation performed at 90 degrees of abduction causes the posterior band and axillary pouch to fan out and cradle the humeral head posteriorly, restricting posterior subluxation of the humeral head.99,114 Tightness of the posterior capsular ligamentous structures has been hypothesized to cause glenohumeral internal rotation deficit (GIRD) and a higher incidence of SLAP (superior labral anterior-posterior) lesions.120 GIRD is defined as the loss (in degrees) of glenohumeral internal rotation of the throwing shoulder compared with the nonthrowing shoulder, as measured in the supine position at 90 degrees of abduction. SLAP lesions were first described by Snyder and coworkers.121 Andrews and colleagues122 have hypothesized that during the follow-through phase of pitching, the biceps contracts eccentrically to decelerate the extending elbow. The resulting force might transmit proximally to the glenoid tubercle and stress, if not tear, the anterosuperior labrum. Burkhart and Morgan123 have proposed that pitchers and overhead athletes develop SLAP lesions because of the peel back mechanism. In a series of 53 overhead athletes who had surgery for type II SLAP lesions, they quantified a loss of internal rotation at 90 degrees of abduction of 25 degrees or greater. They proposed that the tight posteroinferior capsule wraps inferiorly when the arm is in the late cocking phase (90 degrees of abduction and full external rotation [ER]), resulting in the humeral head to shift or be pushed superiorly and posteriorly.123 Additionally, the long head of the biceps is oriented vertically and posteriorly and, as it contracts, it causes the posterior-superior labrum to peel back over the glenoid rim.
Dynamic Stability
Conclusion Understanding the unique position-related constraining characteristics of the glenohumeral ligaments, the clinician can gain insight into capsuloligamentous pathology and anatomic appreciation of the unstable shoulder. The interdependency of the capsuloligamentous-labral complex becomes evident when examining the literature; thus, it can be concluded that the complex should be considered a functional unit.8 With regard to anterior stability with the arm at 0 degrees abduction, the SGHL and MGHL are the primary restraints, with the posterior capsule as the secondary restraint.124 At 45 degrees of abduction, the primary restraint is the MGHL, with secondary restraints being the posterior capsule, IGHL, and MGHL. With the arm at 90 degrees, the primary restraint is the IGHL and secondary restraints are the MGHL and posterior capsule. The IGHL appears to function in a dual role; it is the main restraint against anterior humeral head displacement when in external rotation at 90 degrees of abduction and also forms a substantial posterior barrier when the arm is
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The dynamic system of the glenohumeral joint is the fourth line of defense against shoulder instability (see Fig. 2-13). The musculotendinous units surrounding the glenohumeral joint assist the static restraints in stabilizing responsibilities, while also providing the power for motion. Under normal conditions, forces transmitted by the supraspinatus, infraspinatus, teres minor, and subscapularis provide significant stability to the glenohumeral joint. This is achieved in several ways: 1. Contraction of these muscles centralizes the humeral head in the glenoid by increasing compressive forces.11,16,35,70,79,98 2. The tension developed across the cuff tendons during a contraction squeezes the humeral head preventing anterior and posterior displacement.70 3. Passive tension of the tendons provides some stability.101,104 Active stability is achieved through coordinated shoulder muscle activity that compresses the humeral head into the glenoid and allows concentric rotation of the humeral head on the glenoid (Fig. 2-16).16,71,92,115,125-127 This mechanism, termed concavity-compression, depends on both shoulder muscle forces and the shape of the articular surfaces, principally the glenoid.94 The shoulder muscles may be the primary stabilizers of the glenohumeral joint during the midranges of motion, in which the capsuloligamentous structures are lax. Concavity-compression may also be important at the end ranges of motion, because glenohumeral joint forces are increased.127-129 Shoulder muscle activity protects the capsuloligamentous structures at the end ranges by limiting the joint’s range of motion130 and decreasing strain on these structures.
Figure 2-16. Dynamic effect of the rotator cuff causing compression as well as superior, anterior, and posterior barrier effects. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 85.)
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The effectiveness of the concavity-compression mechanism depends on characteristics of the shoulder muscle forces and the articular surfaces.94 Muscle forces acting on the shoulder joint can be divided into three components— compressive forces, superiorly-inferiorly directed forces, and anteriorly-posteriorly directed forces. The compressive forces stabilize the glenohumeral joint and the anteriorly, posteriorly, inferiorly, and superiorly directed forces, or translational forces, destabilize the glenohumeral joint.127 Glenohumeral joint stability may be quantified by the ratio between the translational forces in any direction and the compressive forces.96 As the ratio between the translational forces and compressive forces decreases, stability of the glenohumeral joint increases, and vice versa.95 Glenohumeral joint stability through concavity-compression is greater in neutral than in an abducted position, which may contribute to the dislocation of the shoulder anteriorly. The rotator cuff muscles and long head of the biceps actively compress the humeral head into the glenoid cavity, along with the outer sleeve of the shoulder muscles, such as the deltoid, pectoralis major, and latissimus dorsi. Shoulders with weakened or deficient rotator cuff mechanisms are likely to have compromised stability from impaired concavity-compression.88 Although the rotator cuff muscles, along with the deltoid, are considered stabilizers of the glenohumeral joint, the subscapularis is considered important for anterior integrity. DePalma and colleagues131 have advocated that the role of the subscapularis is to provide a “dynamic buttress” effect. Morrey and Chao98 have calculated forces at the glenohumeral joint during 90 degrees of coronal plane abduction in external rotation and determined that the anterior shear force increases from 12 to 42 kg in the unloaded upper extremity when the arm moves into 30 degrees of horizontal abduction. The combined tensile strength of the subscapularis and capsuloligamentous complex is calculated as 120 kg,90 allowing stability of the glenohumeral joint to be maintained. Anterior shear increases under higher speeds and greater loads and, when the force exceeds the tensile strength of the anterior structures, dislocation occurs.8 With an incompetent capsuloligamentous complex, the subscapularis muscle becomes the primary structure to stabilize against the impeding translation. This becomes increasingly difficult for the subscapularis with subsequent dislocations because evidence of tendon lengthening has been reported.131-133 Inherent lengthening of this structure leads to inefficient translation of tension from the muscle to bone and the buttress effect is lost. Turkel and coworkers’104 sequential incising study has revealed a significant increase (mean 18 degrees) in external rotation in the neutral position once the subscapularis is cut. No significant increase in anterior translation is noted at 45 and 90 degrees of abduction and the joint cannot be dislocated. These findings were similar to those of Oversen and Nielsen.101 Interestingly, the inferior border of the subscapularis was noted to rise above the inferior humeral
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head at 90 degrees of abduction and external rotation; thus, the subscapularis is an ineffective barrier against dislocation in this position. This finding provides insight as to why patients with a deficient CLC, Bankart lesion, or both recurrently dislocate in the abducted and externally rotated position, even though they possess significant strength of the subscapularis.8 Karduna and associates125 have concluded that activation of the rotator cuff muscles serves to limit rotation and translation of the glenohumeral joint compared with passive positioning. Cain and coworkers,130 using abducted cadaveric shoulders under passive external rotation, have demonstrated that the strain on the inferior glenohumeral ligament is decreased by increasing the force applied to the tendons of the infraspinatus and teres minor. However, muscle forces may promote anterior humeral head translation in the apprehension position, and predispose the glenohumeral joint to anterior instability when other stabilizing mechanisms are not functioning normally.134 Graichen and colleagues79 have found a decrease in glenohumeral translation with active shoulder motion because muscular activity centralizes that humeral head when compared with passive motion. A 50% decrease in the rotator cuff muscle force results in an almost 50% increase in anterior displacement of the humeral head in response to external loading at all glenohumeral joint positions.129 Mild recruitment of the internal rotators, including the subscapularis, has been shown to create an anterior translation constraint in the apprehension position.135 The role of the posterior rotator cuff structures is to assist dynamically in anterior stability of the glenohumeral joint. Cain and associates130 have demonstrated that the posterior cuff, particularly the infraspinatus and teres minor, pull the humeral head posteriorly when contracting, therefore reducing the anterior shear. Lee and coworkers136 have found that the infraspinatus and teres minor generate posterior shear forces and increase compressive forces in the anterior instability position, thereby enhancing joint stability. Conversely, the supraspinatus generates a large anterior shear force in the apprehension position, which may destabilize the joint anteriorly. Combined contraction of the subscapularis and infraspinatus forms a force couple, providing stability throughout the midranges of elevation.88 Electromyography has demonstrated that the subscapularis and infraspinatus contract to stabilize the glenohumeral joint in abduction at 60 to 150 degrees.131 This type of activity, in conjunction with known decreased tensile strength of the rotator cuff,90 explains the high incidence of rotator cuff tears in individuals older than 45 years when they anteriorly dislocate137; excessive translation in the presence of a degenerative cuff causes tearing. Tear location has the most significant effect on stability in the inferior and anterior directions for smaller tears and on the anterior direction for larger tears.88
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Passive tension of the posterior cuff may also play a role in stability. With incision of the infraspinatus and teres minor, significant posterior displacement occurs.101 It could logically be concluded that if passive tension of these muscles maintains significant stability, then active contraction would further enhance stability.8 Saha70 concluded the infraspinatus and teres minor are horizontal steerers that maintain stability. The importance of the posterior rotator cuff and deltoid to posterior stability is seen clinically; patients with posterior instability have responded well with external rotation strengthening.138 This is particularly true if the patient is a subluxator as opposed to a dislocator.139
humeral head translation and the effect of capsular venting and found a slight increase in anterior translation during flexion and horizontal adduction. Matsen and coworkers132 have described this phenomenon as disruption of “finite joint volume.” Finite joint volume combined with the adhesion-cohesion mechanism enhances joint stability.8 Adhesion is described as fluid holding to a surface, whereas cohesion is the joining of two surfaces by fluid. Adhesion-cohesion is best demonstrated by wet microscope slides sticking together but able to slide on one another. The glenohumeral joint mimics this phenomenon at the contact area between the humerus and glenoid.
Lee and An140 have quantified the contribution of the deltoid muscle to glenohumeral joint stability. At 60 degrees of abduction in the scapular plane, deltoid activity increases glenohumeral joint stability; however, at 60 degrees of abduction in the coronal plane, deltoid activity is found to decrease glenohumeral joint stability. Strengthening the middle and posterior portions of the deltoid may provide more stability to a patient with anterior instability, because they may work to generate higher compressive force and lower shear force than the anterior head.
To summarize, the interplay of the various active and passive components contributes to the stability of the glenohumeral joint. The IGHL appears to be the primary structure in providing anterior stability, with the subscapularis contributing to anterior stability through the compressive forces imparted on the joint. The labrum is significant, being the weak link in the chain attaching the IGHL to the bony glenoid rim.8 Regardless of the direction of shoulder instability, efficient control of the rotator cuff is essential to function. Posterior stability is dependent on the anterior capsule and structures. Accepting the capsuloligamentous-labral complex as a functional unit explains why global laxity of this complex leads to multidirectional instability and why a capsular shift surgical procedure is required to address global laxity. Finally, atmospheric pressure and the adhesioncohesion mechanism also add to the stability of the shoulder joint. The clinician needs to consider all factors related to glenohumeral instability to implement safe and effective treatment during conservative and postoperative rehabilitation of the athlete.
The superior labrum serves as an attachment for the long head of the biceps and the superior glenohumeral ligament.61 The long head of the biceps tendon has an important role as a dynamic restraint to external rotation in the abducted shoulder.117 It has been suggested that the biceps becomes more important than the rotator cuff as an anterior stabilizer with decreased stability of the capsuloligamentous structures.141 Injury may represent a traction phenomenon, secondary to activity in the biceps, or possibly a compression phenomenon.88 Repetitive movement into extreme external rotation may excessively load the biceps tendon and predispose the overhead athlete to a biceps-labral complex injury, as noted earlier.142 As long as the scapula is positioned so that the glenoid fossa accepts the net forces acting on the humeral head, the glenohumeral joint will remain stable.88 A redundant capsule may allow excessive glenohumeral angles that exceed the scapulohumeral balancing mechanism,143 allowing instability to occur before the capsuloligamentous structures have sufficiently tightened to provide restraint.
Other Stabilizing Factors Other forces that influence shoulder stability are atmospheric pressure and the adhesion-cohesion mechanism. Normal negative intra-articular pressure has been demonstrated to contribute to the stability of the glenohumeral joint.78 Kumar and Balasubramaniam144 have radiographically demonstrated significant inferior subluxation following percutaneous puncture of the capsule without dependence on muscle suspension, allowing atmospheric air to enter the joint. Harryman and associates72 have evaluated
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MUSCLE ACTIVITY Oatis21 has classified the muscles of the shoulder complex into axioscapular, axioclavicular, scapulohumeral, and axiohumeral muscles. Box 2-1 presents a listing of these categories.
Axioscapular and Axioclavicular Muscles of the axioscapular and axioclavicular groups all attach to both the axioskeleton and scapula or clavicle.21 These muscles act on the sternoclavicular and scapulothoracic joints, and ultimately on the acromioclavicular joint. They provide a stable yet mobile base from which the glenohumeral joint and associated muscles can function. Loss of these muscles, particularly the trapezius or serratus anterior, consequently affects scapulohumeral rhythm and shoulder function. Functional stability of the scapula requires optimal positioning, smooth muscular balance in the force couple around the scapula, and correct timing of muscle activity of the scapula
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BOX 2-1.
Muscles Acting on the Shoulder Complex
Axioscapular and Axioclavicular
Teres minor
Trapezius
Subscapularis
Serratus anterior
Teres major
Levator scapulae
Coracobrachialis
Rhomboid major
Axiohumeral
Rhomboid minor
Pectoralis major
Pectoralis major
Latissimus dorsi
Subclavius
Other
Sternocleidomastoid
Biceps brachii
Scapulohumeral
Triceps brachii
Deltoid
Coracobrachialis
Supraspinatus
Omohyoid
Infraspinatus
rotators.145 A force couple is defined as equal forces producing a rotation by pulling in the opposite direction. The serratus anterior and trapezius force couple is a key component for normal function of the shoulder (Fig. 2-17). This force couple serves four paramount functions:8 (1) rotates the scapula, maintaining the glenoid surface in an appropriate position; (2) through scapular rotation, positions the deltoid to maintain efficient length, thereby enhancing power and stability (without scapular rotation, only 90 degrees of active abduction is available35,146); (3) prevents impingement of the subacromial structures on the coracoacromial arch; and (4) provides a stable base, enabling the axiohumeral and scapulohumeral muscles to move the arm against resistance.88 Trying to move the humerus without the trapezius, serratus, or both is analogous to trying to push against a solid wall while on roller skates.8 This force couple can be divided into upper and lower components, both of which function in all planes of elevation. The upper component is comprised of the upper trapezius, levator scapulae, and upper portion of the serratus anterior. The lower component is comprised of the lower trapezius and lower portion of the serratus anterior.35 For the upper component, the upper trapezius and levator scapulae act to elevate the scapula during shoulder elevation. Activity of the upper trapezius, which is fairly constant in flexion and abduction, continues in a linear fashion as the scapula rotates about its axis.35,147 The upper trapezius is active as a scapular elevator and rotator through its insertion at the acromion. The fibers of the upper portion of the serratus anterior also assist in upward rotation.
Figure 2-17. Serratus anterior (SA) and trapezius force couple generating scapular rotation. LS, levator scapulae; LT, lower trapezius; MT, middle trapezius; UT, upper trapezius. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 100.)
For the lower component, the lower trapezius pulls inferiorly from its insertion at the base of the scapular spine to direct
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the glenoid upward. The lower trapezius contribution increases with increasing abduction. In flexion, activity plateaus between 70 and 120 degrees, after which activity significantly increases to coincide with the abduction curve.35,147 The force couple is now complete as the serratus anterior lower fibers pull the inferior angle forward and laterally. The scapula translates forward on the thoracic wall, directing the glenoid toward the sagittal plane, with the serratus anterior pulling the scapula forward. Progressive activity of the serratus anterior with humeral elevation should contribute to posterior tipping and external rotation of the scapula, as well as upward rotation.29 Electromyographic activity is equal for the scapular rotators at end range flexion and abduction, because the scapula always achieves the same terminal position with elevation, regardless of plane.148 The differences of scapular migration between flexion and coronal plane abduction are explained by the differences in activity of the lower trapezius, middle trapezius, and rhomboids; all have greater action potential values in abduction.8 The downward and medially directed fibers of the lower trapezius may assist in producing posterior tipping and external rotation moments as the humerus is elevated. Individuals with impingement have been shown to exhibit decreased levels of serratus anterior activity and scapular upward rotation34 and a delay in middle and lower trapezius activation.145 A delayed response of the middle and lower trapezius muscles compared with the upper trapezius may lead to supremacy of the upper trapezius muscle, causing an abnormality in scapulohumeral rhythm. The upper and lower trapezius and serratus anterior muscles play a role in the production of scapular upward rotation throughout the range.33 Clinically, a long thoracic nerve palsy is more common, and results in greater functional impairment, than a spinal accessory nerve palsy.8 A prolonged, complete trapezius palsy can be debilitating because of the loss of scapular suspension and subsequent depression of the shoulder girdle (Fig. 2-18). A patient with an isolated spinal accessory nerve palsy will demonstrate weak sagittal plane motion, but frontal plane abduction will be significantly impaired. With a complete long thoracic nerve palsy, patients typically will be unable to flex or abduct the involved shoulder fully. A synergy also exists between the scapular adductors, particularly the middle and lower trapezius, with the motion of external rotation. When resisting shoulder external rotation in neutral, the trapezius and rhomboids work to stabilize the vertebral border of the scapula.8 In individuals with a spinal accessory nerve palsy, this relation becomes evident. Resisted external rotation results in a flip sign because the middle and lower trapezius cannot oppose the pull of the external rotators from their fixed origins.149,150 Clinically, we have seen up to a 25% reduction of internal and external torque output in patients with a
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Figure 2-18. Patient with chronically denervated trapezius. Note shoulder girdle depression caused by loss of trapezius suspension effect.
serratus anterior or trapezius nerve palsy caused by loss of this synergy. Recognition of scapulothoracic contribution to shoulder function is imperative. The clinician must evaluate for scapulothoracic muscle dysfunction because significant impairment of these muscles often exists in the presence of shoulder pathology. A muscular imbalance from weakness or shortening can result in impaired stabilization of the scapula. This concept becomes especially important for the thrower, who depends on the proper coordination and sequencing of the entire shoulder complex.
Scapulohumeral Muscles The scapulohumeral muscles provide motion and dynamic stabilization to the glenohumeral joint.10,19,21 These muscles are crucial for function of the shoulder complex because the glenohumeral joint contributes to a significant amount of motion. In the normal shoulder, the middle deltoid is active in all planes of elevation,128,151-153 whereas the anterior and posterior heads command flexion and extension, respectively.8 Although the anterior fibers dominate motion in flexion, the middle fibers become more involved at 60 degrees.147 This occurs because of relative humeral realignment toward the scapular plane as the scapula translates forward over the thoracic wall. Also, the obligatory internal rotation with flexion moves the deltoid’s insertion forward, providing the middle deltoid with a more efficient line of pull. Poppen and Walker128 have found that as the line of pull improves, so does the deltoid moment arm. The improvement in the line of pull and moment arm during abduction would be meaningless to the deltoid if the scapula did not rotate, functionally lengthening the deltoid. Without scapular rotation, the deltoid would excessively shorten by 90 degrees of abduction and the arm could not actively raise past this point; this is called active insufficiency.35,146 The deltoid is able to maximize function by a complex interplay of mechanical adjustments as the insertion rises overhead and the scapula rotates.
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The other component of the scapulohumeral muscles is the rotator cuff, which provides the core dynamic control about the glenohumeral joint. Comprised of four muscles and associated tendons, the rotator cuff dynamically maintains articular congruity, thus providing the larger and more powerful shoulder muscles with the ability to move against great resistance.8 The dynamic effect of the supraspinatus is to stabilize the humeral head in the glenoid fossa centrally.5,11,35,70,98,128,154 This muscle also provides a depressive force because of tendon compression of the superior humeral head.155,156 A dysfunctional rotator cuff is unable to mitigate the upward shear from the deltoid, leading to impingement of the supraspinatus tendon and subacromial bursa against the coracoacromial arch.42 This mechanism may lead to humeral head superior migration in patients with chronic rotator cuff tears.157-159 Fatigue of the deltoid and rotator cuff complex also has been found to produce abnormal glenohumeral kinematics of superior migration of the humeral head on the glenoid.160 The second force couple of the shoulder complex is from the action of the deltoid, supraspinatus, infraspinatus, teres minor, and subscapularis (Fig. 2-19). The line of pull to the glenoid face of the infraspinatus and subscapularis has been estimated at 45 degrees, and the teres minor at 55 degrees.5 These three muscles have a negligible moment arm as abductors.33 Their responsibility in the force couple is to exert a predominantly downward shear, which peaks at 60 degrees of elevation, as well as a compressive load.3,35,70 As the deltoid draws the humeral head upward, the depressors tug downward, allowing humeral rotation while maintaining glenohumeral joint conformity.74,128 Compromise of the humeral head depressors results in an
imbalanced struggle against the opposing deltoid shear, leading to superior humeral head displacement, loss of the effective fulcrum, and impaired strength. The supraspinatus and deltoid are in optimal alignment in the scapular plane.12 The supraspinatus is active in all planes of elevation,35,147,151,153 contrary to its originally being regarded as the isolated initiator of abduction. This has been clearly disproved by electromyographically induced nerve palsy studies162-164 and clinical observations.165,166 In fact, 40% to 60% of elevation torque output has been attributed to the supraspinatus and infraspinatus.167 With scapular plane elevation of the glenohumeral joint, the supraspinatus pulls the humeral head into the glenoid cavity and remains active during the movement.168 Scepi and colleagues168 have determined that at the beginning of scapular plane elevation, the anterior portion of the deltoid works synergistically with the supraspinatus. There remains some controversy over the stabilizing versus abducting effect. Celli and associates169 have defined a stabilizer as a structure that demonstrates constant activity by electromyography compared with a mover, whose activity increases with motion. It was found that the deltoid is the abducting force (mover) whereas the supraspinatus is a stabilizer. Ito147 has found a linear progression of electrical activity in the supraspinatus and deltoid during abduction. The infraspinatus and teres minor have also been found to be active throughout elevation,35,151,153 fulfilling two responsibilities—force couple requirements and serving as a posterior barrier against translation. The infraspinatus also contributes to the generation of abduction glenohumeral torque and stabilization of the humeral head against superior subluxation.170 The infraspinatus demonstrates a linear progression in activity throughout coronal35 and scapular plane abduction.70,147 Activity differs somewhat in flexion, being higher and peaking at between 60 and 120 degrees. Activity is enhanced because of muscle demand created when the elbow is flexed to 90 degrees, producing a moment toward internal rotation.8 The subscapularis acts synergistically with the posterior cuff muscles to depress and compress the humeral head and is more active in abduction than flexion. Significant activity of the teres minor and infraspinatus is noted in full external rotation and horizontal extension.171-173 This is the late cocking phase position in throwing and is advocated for strengthening the posterior cuff muscles.174 Strong eccentric activity occurs in the subscapularis during the late cocking phase of throwing.171,175 Further discussion of the throwing cycle and pitching mechanics will be presented in subsequent chapters..
Figure 2-19. Deltoid and rotator cuff force couple. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 92.)
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Clinically, strengthening of the posterior cuff muscles is essential for rehabilitating the nonoperative and postoperative athlete. Proper strength and balance of these muscles are key components of optimal shoulder function.
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Axiohumeral Muscles The axiohumeral muscles, pectoralis major and latissimus dorsi, attach the thorax to the humerus.21 They have large physiologic cross-sectional areas and are believed to provide additional strength to shoulder movement.113 Controversy exists regarding activity of the latissimus dorsi and pectoralis muscles in unresisted rotation.8 These muscles produce the forces required to accelerate the arm and object velocity.
Other Muscles The biceps brachii, coracobrachialis, and triceps brachii also act on the shoulder joint. The biceps, although predominantly an elbow flexor and forearm supinator, can be an effective elevator and functions to stabilize the humeral head in the glenoid, preventing upward migration.85,146,176 Also, humeral external rotation places the long head laterally, causing it to act like a pulley and assisting in arm elevation.
SUMMARY This chapter has discussed the biomechanics and principals behind the function of the shoulder complex. There is an impressive interdependency among muscle action, ligamentous stability, and osseous orientation to shoulder function. Understanding this relationship is paramount to the successful diagnosis and treatment of shoulder pathology and dysfunction. References 1. Culham E, Peat M: Functional anatomy of the shoulder complex. J Orthop Sports Phys Ther 18:342-350, 1993. 2. Bearn JG: Direct observations on the function of the capsule of the sternoclavicular joint in clavicular support. J Anat 101:159-170, 1967. 3. Bateman J: The Shoulder and Neck. Philadelphia, WB Saunders, 1971. 4. Steindler A: Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, Ill, Charles C Thomas, 1955. 5. Perry J: Biomechanics. In Rowe C (ed): The Shoulder. New York, Churchill-Livingstone, 1988. 6. Calliet R: Shoulder Pain. Philadelphia, FA Davis, 1977. 7. Kebaetse M, McClure P, Pratt NA: Thoracic position effect on shoulder range of motion, strength, and three-dimensional scapular kinematics. Arch Phys Med Rehabil 80:945-950, 1999. 8. Kelley M, Clark W: Orthopedic Therapy of the Shoulder. Philadelphia, JB Lippincott, 1995. 9. Burkhart SS, Morgan CD, Kibler WB; The disabled throwing shoulder: Spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19:641-661, 2003. 10. Kibler WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998.
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11. Codman E: The Shoulder. Boston, Thomas Todd, 1934. 12. Johnston T: The movements of the shoulder joint. A plea for the use of the “Plane of the Scapula” as the plane of reference in movements occurring in the humero-scapular joint. Br J Surg 25:252, 1937. 13. Saha AK: Theory of Shoulder Mechanism: Descriptive and Applied. Springfield, Ill, Charles C Thomas, 1961. 14. Doody SG, Freedman L, Waterland JC: Shoulder movements during abduction in the scapular plane. Arch Phys Med Rehabil 51:595-604, 1970. 15. Freedman L, Munro RR.: Abduction of the arm in the scapular plane: Scapular and glenohumeral movements. A roentgenographic study. J Bone Joint Surg Am 48:1503-1510, 1966. 16. Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 58:195-201, 1976. 17. Dvir Z, Berme N: The shoulder complex in elevation of the arm: A mechanism approach. J Biomech 11:219-225, 1978. 18. McGregor L: Rotation at the shoulder: A critical injury. Br J Surg 24:425-438, 1937. 19. Rowe CR, Sakellarides HT: Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop 20:40-48, 1961. 20. Michener LA, McClure PW, Karduna AR: Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech (Bristol, Avon) 18:369-379, 2003. 21. Oatis CA: Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Lippincott Williams & Wilkins, 2004. 22. De Freitas V, Vitti M, Furlani J: Electromyographic study of levator scapulae and rhomboideus major muscles in movements of the shoulder and arm. Electromyogr Clin Neurophysiol 20:205-216, 1980. 23. Duchenne G, Kaplan E: Physiology of Motion. Philadelphia, JB Lippincott, 1949. 24. Kendall F, McCreary E: Muscle Testing and Function, 3rd ed. Baltimore, Williams & Wilkins, 1982. 25. Karduna AR, McClure PW, Michener LA: Scapular kinematics: Effects of altering the Euler angle sequence of rotations. J Biomech 33:1063-1068, 2000. 26. van der Helm FC: A finite element musculoskeletal model of the shoulder mechanism. J Biomech 27:551-569, 1994. 27. Borstad JD, Ludewig PM: Comparison of scapular kinematics between elevation and lowering of the arm in the scapular plane. Clin Biomech (Bristol, Avon) 17:650-659, 2002. 28. Karduna AR, McClure PW, Michener LA, Sennett B: Dynamic measurements of three-dimensional scapular kinematics: A validation study. J Biomech Eng 123:184-190, 2001. 29. Ludewig PM, Cook TM, Nawoczenski DA: Three-dimensional scapular orientation and muscle activity at selected positions of humeral elevation. J Orthop Sports Phys Ther 24:57-65, 1996. 30. Lukasiewicz AC, McClure P, Michener L, et al: Comparison of three-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29:574-583, 1999. 31. McClure PW, Michener LA, Sennett BJ, Karduna AR: Direct three-dimensional measurement of scapular kinematics during dynamic movements in vivo. J Shoulder Elbow Surg 10:269-277, 2001. 32. McQuade KJ, Smidt GL: Dynamic scapulohumeral rhythm: The effects of external resistance during elevation of the
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arm in the scapular plane. J Orthop Sports Phys Ther 27:125-133, 1998. Ebaugh DD, McClure PW, Karduna AR: Three-dimensional scapulothoracic motion during active and passive arm elevation. Clin Biomech (Bristol, Avon) 20:700-709, 2005. Ludewig PM, Cook TM: Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 80:276-291, 2000. Inman V, Saunder J, Abbot L: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1, 1944. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Indian J Surg 12:153-165, 1950. Graichen H, Stammberger T, Bonel H, et al: Magnetic resonance-based motion analysis of the shoulder during elevation. Clin Orthop Relat Res (370):154-163, 2000. Myers JB, Laudner KG, Pasquale MR, et al: Scapular position and orientation in throwing athletes. Am J Sports Med 33:263-271, 2005. Paletta GA Jr, Warner JJ, Warren RF, et al: Shoulder kinematics with two-plane x-ray evaluation in patients with anterior instability or rotator cuff tearing. J Shoulder Elbow Surg 6:516-527, 1997. Warner JJ, Micheli LJ, Arslanian LE, et al: Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. A study using Moire topographic analysis. Clin Orthop Relat Res (285):191-199, 1992. Kibler WB, Uhl TL, Maddux JW, et al: Qualitative clinical evaluation of scapular dysfunction: a reliability study. J Shoulder Elbow Surg 11:550-556, 2002. Mell AG, LaScalza S, Guffey P, et al: Effect of rotator cuff pathology on shoulder rhythm. J Shoulder Elbow Surg 14(Suppl):58S-64S, 2005. von Eisenhart-Rothe R, Matsen FA 3rd, Eckstein F, et al: Pathomechanics in atraumatic shoulder instability: Scapular positioning correlates with humeral head centering. Clin Orthop Relat Res (433):82-89, 2005. Finley MA, Lee RY: Effect of sitting posture on threedimensional scapular kinematics measured by skinmounted electromagnetic tracking sensors. Arch Phys Med Rehabil 84:563-568, 2003. Smith J, Kotajarvi BR, Padgett DJ, Eischen JJ: Effect of scapular protraction and retraction on isometric shoulder elevation strength. Arch Phys Med Rehabil 83:367-370, 2002. Borstad JD, Ludewig PM: The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J Orthop Sports Phys Ther 35:227-238, 2005. Stokdijk M, Eilers PH, Nagels J, Rozing PM: External rotation in the glenohumeral joint during elevation of the arm. Clin Biomech (Bristol, Avon) 18:296-302, 2003. Ahmad CS, Wang VM, Sugalski MT, et al: Biomechanics of shoulder capsulorrhaphy procedures. J Shoulder Elbow Surg 14(Suppl):12S-18S, 2005. Hawkins RJ, Angelo RL: Glenohumeral osteoarthrosis. A late complication of the Putti-Platt repair. J Bone Joint Surg Am 72:1193-1197, 1990. Lusardi DA, Wirth MA, Wurtz D, Rockwood CA Jr: Loss of external rotation following anterior capsulorrhaphy of the shoulder. J Bone Joint Surg Am 75:1185-1192, 1993.
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51. Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49-70, 1965. 52. Moseley HF: The clavicle: Its anatomy and function. Clin Orthop 58:17-27, 1958. 53. Cave A: The nature and morphology of the costoclavicular ligament. J Anat 95:170-179, 1961. 54. McArdle PJ, Kalbassi R, Ilankovan V: Stability of the sternoclavicular joint. A retrospective study. Br J Oral Maxillofac Surg 41:12-15, 2003. 55. Spencer EE, Kuhn JE, Huston LJ, et al: Ligamentous restraints to anterior and posterior translation of the sternoclavicular joint. J Shoulder Elbow Surg 11:43-47, 2002. 56. Shaffer BS: Painful conditions of the acromioclavicular joint. J Am Acad Orthop Surg 7:176-188, 1999. 57. Basmajian J, Bazant F: Factors preventing downward dislocation of the adducted shoulder joint. An electromyographic and morphological study. Am J Orthop 41A:1182-1186, 1959. 58. Kennedy JC, Cameron H: Complete dislocation of the acromio-clavicular joint. J Bone Joint Surg Br 36:202-208, 1954. 59. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Rockwood CA, Matsen FA 3rd (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 413-416. 60. Kapandji I: The Physiology of Joints, vol 1. Baltimore, Williams & Wilkins, 1970. 61. Curl LA, Warren RF: Glenohumeral joint stability. Selective cutting studies on the static capsular restraints. Clin Orthop Relat Res (330):54-65, 1996. 62. DePalma A: Surgery of the Shoulder. New York, JB Lippincott, 1973. 63. Blakely RL, Palmer ML: Analysis of rotation accompanying shoulder flexion. Phys Ther 64:1214-1216, 1984. 64. MacConail M, Basmajian J: Muscles and Movements: A Basis for Human Kinesiology. Baltimore, Williams & Wilkins, 1969. 65. Howell SM, Galinat BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop Relat Res (243): 122-125, 1989. 66. Iannotti JP, Gabriel JP, Schneck SL, et al: The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am 74:491-500, 1992. 67. Soslowsky LJ, Flatow EL, Bigliani LU, et al: Quantitation of in situ contact areas at the glenohumeral joint: A biomechanical study. J Orthop Res 10:524-534, 1992. 68. Van der Helm FC, Veeger HE, Pronk GM, et al: Geometry parameters for musculoskeletal modelling of the shoulder system. J Biomech 25:129-144, 1992. 69. Kaltenborn F: Mobilization of the Extremity Joints. Examination and Basic Treatment Techniques. Oslo, Olaf Bokhandel, 1980. 70. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491-505, 1971. 71. Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232, 1988. 72. Harryman DT 2nd, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990. 73. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992.
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74. Kelkar R, Flatow E, Bigliani L, et al: A stereophotogrammetric method to determine the kinematics of the glenohumeral joint. Adv Bioeng 19:143-145, 1992. 75. Yamaguchi K, Sher JS, Andersen WK, et al: Glenohumeral motion in patients with rotator cuff tears: A comparison of asymptomatic and symptomatic shoulders. J Shoulder Elbow Surg 9:6-11, 2000. 76. Nobuhara K: The Shoulder: Its Function and Clinical Aspects. Tokyo, Igaku-Shoin, 1977. 77. Werner CM, Nyffeler RW, Jacob HA, Gerber C: The effect of capsular tightening on humeral head translations. J Orthop Res 22:194-201, 2004. 78. Moore SM, Musahl V, McMahon PJ, Debski RE: Multidirectional kinematics of the glenohumeral joint during simulated simple translation tests: Impact on clinical diagnoses. J Orthop Res 22:889-894, 2004. 79. Graichen H, Stammberger T, Bonel H, et al: Glenohumeral translation during active and passive elevation of the shoulder—a 3D open-MRI study. J Biomech 33:609-613, 2000. 80. Moseley HF, Overgaard D: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913-927, 1962. 81. Novotny JE, Woolley CT, Nichols CE 3rd, Beynnon BD: In vivo technique to quantify the internal-external rotation kinematics of the human glenohumeral joint. J Orthop Res 18:190-194, 2000. 82. Bigliani LU, Kelkar R, Flatow EL, et al: Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res (330):13-30, 1996. 83. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop (285): 181-190, 1992. 84. Jobe CM, Iannotti JP: Limits imposed on glenohumeral motion by joint geometry. J Shoulder Elbow Surg 4:281-285, 1995. 85. Kent BE: Functional anatomy of the shoulder complex. Phys Ther 51:867-874, 1971. 86. Peat M: Functional anatomy of the shoulder complex. Phys Ther 66:1855-1865, 1986. 87. Sarrafian SK: Gross and functional anatomy of the shoulder. Clin Orthop Relat Res (173):11-19, 1983. 88. Abboud JA, Soslowsky LJ: Interplay of the static and dynamic restraints in glenohumeral instability. Clin Orthop Relat Res (400):48-57, 2002. 89. Rowe CR: The Shoulder. New York, Churchill-Livingstone, 1988. 90. Reeves B: Experiments on the tensile strength of the anterior capsular structures of the shoulder in man. J Bone Joint Surg Br 50:858-865, 1968. 91. Hara H, Ito N, Iwasaki K: Strength of the glenoid labrum and adjacent shoulder capsule. J Shoulder Elbow Surg 5:263-268, 1996. 92. Bankart A: The pathology and treatment of recurrent dislocation of the shoulder. Br J Surg 26:23-29, 1938. 93. Rowe CR, Patel D, Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 94. Lippitt SB, Vanderhoof JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quanitative analysis. J Shoulder Elbow Surg 2: 27-34, 1993.
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95. Halder AM, Kuhl SG, Zobitz ME, et al: Effects of the glenoid labrum and glenohumeral abduction on stability of the shoulder joint through concavity-compression: An in vitro study. J Bone Joint Surg Am 83:1062-1069, 2001. 96. Lazarus MD, Sidles JA, Harryman DT 2nd, Matsen FA 3rd: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 97. Rodosky MW, Harner CD, Fu FH: The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med 22:121-130, 1994. 98. Morrey BF, Chao EY: Recurrent anterior dislocation of the shoulder. In Dumbleton J, Black J (eds): Clinical Biomechanics. London, Churchhill Livingstone, 1981. 99. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 100. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 101. Ovesen J, Nielsen S: Anterior and posterior shoulder instability. A cadaver study. Acta Orthop Scand 57:324-327, 1986. 102. Terry GC, Hammon D, France P, Norwood LA: The stabilizing function of passive shoulder restraints. Am J Sports Med 19:26-34, 1991. 103. Townley CO: The capsular mechanism in recurrent dislocation of the shoulder. J Bone Joint Surg Am 32:370-380, 1950. 104. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 105. Flatow EL, Warner JI: Instability of the shoulder:complex problems and failed repairs: Part I. Relevant biomechanics, multidirectional instability, and severe glenoid loss. Instr Course Lect 47:97-112, 1998. 106. Moore SM, McMahon PJ, Azemi E, Debski RE: Bi-directional mechanical properties of the posterior region of the glenohumeral capsule. J Biomech 38:1365-1369, 2005. 107. Clark JM, Harryman DT 2nd: Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. 108. Gerber C, Werner CM, Macy JC, et al: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J Bone Joint Surg Am 85:48-55, 2003. 109. Ferrari DA: Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20-24, 1990. 110. Bowen MK, Warren RF: Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 10:757-782, 1991. 111. Nobuhara K, Ikeda H: Rotator interval lesion. Clin Orthop Relat Res (223):44-50, 1987. 112. Burkart AC, Debski RE: Anatomy and function of the glenohumeral ligaments in anterior shoulder instability. Clin Orthop Relat Res (400):32-39, 2002. 113. Basmajian J: Muscles Alive, 4th ed. Baltimore, Williams & Wilkins, 1979. 114. Gagey OJ, Boisrenoult P: Shoulder capsule shrinkage and consequences on shoulder movements. Clin Orthop Relat Res (419):218-222, 2004.
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115. Blasier RB, Guldberg MS, Rothman ED: Anterior shoulder stability: Contributions of rotator cuff forces and the capsular ligaments in a cadaver model. J Shoulder Elbow Surg 1:140-150, 1992. 116. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298-308, 1995. 117. Kuhn JE, Huston LJ, Soslowsky LJ, et al: External rotation of the glenohumeral joint: Ligament restraints and muscle effects in the neutral and abducted positions. J Shoulder Elbow Surg 14(Suppl):39S-48S, 2005. 118. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 119. Pollock RG, Wang VM, Bucchieri JS, et al: Effects of repetitive subfailure strains on the mechanical behavior of the inferior glenohumeral ligament. J Shoulder Elbow Surg 9:427-435, 2000. 120. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. 121. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990. 122. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901-911, 1991. 123. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 124. Wilk KE, Andrews JR, Arrigo CA: The physical examination of the glenohumeral joint: Emphasis on the stabilizing structures. J Orthop Sports Phys Ther 25:380-389, 1997. 125. Karduna AR, Williams GR, Williams JL, Iannotti JP: Kinematics of the glenohumeral joint: Influences of muscle forces, ligamentous constraints, and articular geometry. J Orthop Res 14:986-993, 1996. 126. Kelkar R, Wang VM, Flatow EL, et al: Glenohumeral mechanics: A study of articular geometry, contact, and kinematics. J Shoulder Elbow Surg 10:73-84, 2001. 127. Labriola JE, Lee TQ, Debski RE, McMahon PJ: Stability and instability of the glenohumeral joint: The role of shoulder muscles. J Shoulder Elbow Surg 14(Suppl): 32S-38S, 2005. 128. Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop Relat Res (135):165-170, 1978. 129. Wuelker N, Korell M, Thren K: Dynamic glenohumeral joint stability. J Shoulder Elbow Surg 7:43-52, 1998. 130. Cain PR, Mutschler TA, Fu FH, Lee SK: Anterior stability of the glenohumeral joint. A dynamic model. Am J Sports Med 15:144-148, 1987. 131. DePalma AF, Cooke AJ, Prabhakar M: The role of the subscapularis in recurrent anterior dislocations of the shoulder. Clin Orthop Relat Res 54:35-49, 1967. 132. Matsen FA 3rd, Thomas SC, Rockwood CA: Anterior glenohumeral instability. In Rockwood CA, Matsen FA 3rd (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 526-622. 133. Symeonides PP: The significance of the subscapularis muscle in the pathogenesis of recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 54:476-483, 1972.
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134. Labriola JE, Jolly JT, McMahon PJ, Debski RE: Active stability of the glenohumeral joint decreases in the apprehension position. Clin Biomech (Bristol, Avon) 19:801-809, 2004. 135. McQuade KJ, Murthi AM: Anterior glenohumeral force/ translation behavior with and without rotator cuff contraction during clinical stability testing. Clin Biomech (Bristol, Avon) 19:10-15, 2004. 136. Lee SB, Kim KJ, O’Driscoll SW, et al: Dynamic glenohumeral stability provided by the rotator cuff muscles in the mid-range and end-range of motion. A study in cadavera. J Bone Joint Surg Am 82:849-857, 2000. 137. Hawkins RJ, Misamore GW, Hobeika PE: Surgery for full-thickness rotator-cuff tears. J Bone Joint Surg Am 67: 1349-1355, 1985. 138. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409-419, 1987. 139. Detrisac D, Johnson L: Arthroscopic Shoulder Anatomy. Thorofare, NJ, Slack, 1986. 140. Lee SB, An KN: Dynamic glenohumeral stability provided by three heads of the deltoid muscle. Clin Orthop Relat Res (400):40-47, 2002. 141. Itoi E, Newman SR, Kuechle DK, et al: Dynamic anterior stabilisers of the shoulder with the arm in abduction. J Bone Joint Surg Br 76:834-836, 1994. 142. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14: 553-565, 1998. 143. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980. 144. Kumar VP, Balasubramaniam P: The role of atmospheric pressure in stabilising the shoulder. An experimental study. J Bone Joint Surg Br 67:719-721, 1985. 145. Cools AM, Witvrouw EE, Declercq GA, et al: Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms. Am J Sports Med 31:542-549, 2003. 146. Ito N: Electromyographic study of shoulder joint. Nippon Seikeigeka Gakkai Zasshi 54:1529-1540, 1980. 147. Laumann U: Kinesiology of the shoulder joint. In Kôlbel R, Helbig B, Blauth W (eds): Shoulder Replacement. Berlin, Springer-Verlag, 1987, pp 23-31. 148. Kelley M: Clinical evaluation of the shoulder. In Mackin E, Callahan A, Skirven T (eds): Rehabilitation of the Hand and Upper Extremity, 5th ed. St. Louis, Mosby, 2002, pp 1311-1350. 149. Kelley M, Brenneman S: The scapular flip sign: An examination sign to identify the presence of a spinal accessory nerve palsy. Presented at the APTA Combined Sections Meeting, New Orleans, February 2000. 150. Nuber GW, Bowman ID, Perry JP, et al: EMG analysis of classical shoulder motion. Trans Orthop Res Soc 11, 1986. 151. Shevlin MG, Lehmann JF, Lucci JA: Electromyographic study of the function of some muscles crossing the glenohumeral joint. Arch Phys Med Rehabil 50:264-270, 1969. 152. Sugahara R: Electromyographic study of shoulder movements. Jpn J Rehab Med 11:41-52, 1974.
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153. Lucas DB: Biomechanics of the shoulder joint. Arch Surg 107:425-432, 1973. 154. Radin EL: Biomechanics and functional anatomy. In Post M (ed): The Shoulder: Surgical and Nonsurgical Management, 2nd ed. Philadelphia, Lea & Febiger, 1988, pp 54-60. 155. Matsen FA 3rd: Biomechanics of the shoulder. In Frankel VH, Nordin M (eds): Basic Biomechanics of the Skeletal System. Philadelphia, Lea & Febiger, 1980, pp 221-242. 156. Zuckerman JD, Matsen FA 3rd: Biomechanics of the shoulder. In Zuckerman JD, Matsen FA 3rd (eds): Basic Biomechanics of the Musculoskeletal System. Philadelphia, Lea & Febiger, 1989, pp 225-247. 157. Deutsch A, Altchek DW, Schwartz E, et al: Radiologic measurement of superior displacement of the humeral head in the impingement syndrome. J Shoulder Elbow Surg 5: 186-193, 1996. 158. Hawkins RJ, Bell RH, Hawkins RH, Koppert GJ: Anterior dislocation of the shoulder in the older patient. Clin Orthop Relat Res (206):192-195, 1986. 159. Weiner DS, Macnab I: Superior migration of the humeral head. A radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 52:524-527, 1970. 160. Chen SK, Simonian PT, Wickiewicz TL, et al: Radiographic evaluation of glenohumeral kinematics: A muscle fatigue model. J Shoulder Elbow Surg 8:49-52, 1999. 161. De Duca CJ, Forrest WJ: Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomech 6:385-393, 1973. 162. Colachis SC Jr, Strohm BR: Effect of suprascapular and axillary nerve blocks on muscle force in upper extremity. Arch Phys Med Rehabil 52:22-29, 1971. 163. Colachis SC, Jr., Strohm BR, Brechner VL: Effects of axillary nerve block on muscle force in the upper extremity. Arch Phys Med Rehabil 50:647-654, 1969. 164. Howell SM, Imobersteg AM, Seger DH, Marone PJ: Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am 68:398-404, 1986.
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165. Markhede G, Monastyrski J, Stener B: Shoulder function after deltoid muscle removal. Acta Orthop Scand 56: 242-244, 1985. 166. Staples OS, Watkins AL: Full active abduction in traumatic paralysis of the deltoid. J Bone Joint Surg 25:85, 1943. 167. Kuhlman JR, Iannotti JP, Kelly MJ, et al: Isokinetic and isometric measurement of strength of external rotation and abduction of the shoulder. J Bone Joint Surg Am 74: 1320-1333, 1992. 168. Scepi M, Faure JP, Ridoux N, et al: A three-dimensional model of the shoulder girdle. Forces developed in deltoid and supraspinatus muscles during abduction. Surg Radiol Anat 26:290-296, 2004. 169. Celli L, Balli A, de Luise G, Rovesta C: Some new aspects of the functional anatomy of the shoulder. Ital J Orthop Traumatol 11:83-91, 1985. 170. Mura N, O’Driscoll SW, Zobitz ME, et al: The effect of infraspinatus disruption on glenohumeral torque and superior migration of the humeral head: A biomechanical study. J Shoulder Elbow Surg 12:179-184, 2003. 171. Jobe FW, Moynes DR, Tibone JE, Perry J. An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 172. Kadefors R, Petersen I, Herberts P: Muscular reaction to welding work: An electromyographic investigation. Ergonomics 19:543-548, 1976. 173. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247-270, 1983. 174. Blackburn T, McLeod W, White B, Wofford L: Analysis of posterior rotator cuff exercise. Athl Train 25:40-45, 1990. 175. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 176. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop Relat Res (244):172-175, 1989.
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CHAPTER 3 Standardized Shoulder Examination—
Clinical and Functional Approaches Terry R. Malone
This chapter addresses the components of a standardized examination process for the shoulder. This process requires attention to detail, recognizing the function of the shoulder as that of multiple joints functioning in a complex rather than individual actions at single joints. Most evaluation schemes have been derived through the particular emphases of the individual practitioner.1-4 Most involve an anatomic inspection moving toward a functional examination through range of motion and neurologic assessment, followed by specific tests for particular structures. Fortunately, the contemporary clinician is able to increase the information in this database to include assessment of strength and evaluation of function through a number of techniques. This chapter presents a schema for clinical assessment and a functional process of shoulder evaluation. It is a selective approach, with the focus on clinical tests with higher predictive qualities and how best to apply the results to establish diagnoses and treatment regimens. Radiographic, magnetic resonance imaging, arthrotomographic, and ultrasonographic modes of assessment are discussed in other chapters.
Is the pain acute or chronic? When does it hurt? Do you have pain at night? Do you have pain at rest? What type of pain is present? What has been the effect of treatment: such as rest, heat, ice, and exercise? Have you tried an anti-inflammatory drug? In both sports and work, what do you wish to do, and what are you unable to do? Have you had this problem before? Is there a medical history of diabetes in your family? These are examples of the types of questions that should be asked to get a picture of the condition before proceeding into an objective assessment. Also, as you begin your objective evaluation, it is important to have the person point with one finger to the area of pain. This enables you to determine the location and begin the process of evaluation for referral of pain rather than structure only. Screen. Be certain to look at the cervical spine, because many shoulder problems are related to underlying nerve roots of segmental facilitation and are easily misinterpreted as a peripheral problem. I always look to the capsule after ruling out the spine, particularly in athletes, because capsular insufficiency is common and often missed. The great challenge is to appreciate the need for motion and the changes in the thrower that enable him or her to be successful but also different.
A recommended schema for shoulder evaluation is presented that describes the tests commonly used in the clinical and manual examination of the musculoskeletal shoulder complex. Additional portions of this chapter describe strength assessment—static and dynamic—and culminate in a discussion of functional assessments.
EXAMINATION SCHEMA
General Evaluation Sequence. Clinicians must develop a process that works for them and, in their particular setting, provides information to assess the patient on the initial visit and also allows them to assess treatment effectiveness at ensuing clinical visits. This objective standardized scheme is described in Box 3-1 (also discussed elsewhere in this text). I will focus on the recommended clinical screening process and on the difficult problems of strength assessment and functional performance that is so important for the athlete.
Clinicians must develop an evaluation form or sequence to enable them to be effective and efficient. A written form is helpful to keep the clinician focused and to avoid becoming too findings-oriented. There might be a greater likelihood of reaching a conclusion when an expected positive examination result is confirmed using our hands. The following series of tenets may help in developing an evaluation form or sequence. Initiating the Evaluation. The evaluation should begin with the patient’s subjective description of the chief complaint, such as by asking the following questions:
Clinical Shoulder Screen During the past decade, clinical examination has evolved through the validation of tests to determine whether they are useful. As greater appreciation for the capsule labral complex and interactions of the scapula has been gained, more detailed scrutiny of popular assessment techniques has enabled clinicians to select and apply manual skills for
Why are you here in the clinic? What was the onset of this problem, abrupt or insidious? What is the level of pain? How long has it been hurting? 45
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BOX 3-1.
Objective Standardized Scheme
Observation—position and movement of scapula; rightleft comparisons; scapular slide test when obviously altered or different scapular patterns observed Active motion—elevation, external rotation at side, back scratch for internal rotation (composite movement); recognition of expected compensations in the throwing shoulder (loss of internal rotation and increased external rotation) Palpation—primary bony articulations and prominences Passive motion—done when differences seen actively Resisted motion Joint play Orthopedic tests—used as battery and sequenced; initial screen pattern Strength—isometric through dynamic assessment
applies an inferiorly directed stress through the upper arm to minimize the effect of the biceps and triceps. A markedly large displacement is typical bilaterally in the patient with multidirectional instability. Although there are no specific references related to independent validity of this test, it appears to be valuable as part of an overall assessment and when used as part of a battery of tests.5 Load and Shift Test—Anterior and Posterior Capsule. The load and shift test is designed to assess the anterior and posterior capsules of the glenohumeral joint performed while the subject is in a neutral sitting or supine posture. The examiner stabilizes the scapula with one hand, while displacing or gliding the humeral head with the other, assessing the displacement anteriorly and posteriorly. Hawkins and Schutte6 have provided a grading scale of this process; grade 1 is minimal motion and grade 3 manifests with the head riding up and over the glenoid rim. The validity of this test in demonstrating the presence of a Bankart lesion (anterior instability) is greater than 90% (sensitivity, 90.9%; specificity, 93.3%).7
Functional performance
determining structural problems more effectively. The process of this shoulder screen is to divide patients into two groups and then divide each of these into two subgroupings (Table 3-1). The screen is sequenced to assess the capsule initially. This can help determine whether the patient has presented with an instability or whether there is an underlying instability that has led to a secondary problem related to capsular incompetency. I recommend doing a series of capsular tests begun in the seated position.
Capsular Tests—Recommended Sequence Sulcus Sign (Superior Capsule). The sulcus sign is designed to assess the superior capsular restraints, including the superior glenohumeral ligament and coracohumeral ligament, in an adducted neutral posture. The examiner TABLE 3-1 Shoulder Screen INSTABILITY-RELATED (CAPSULAR TESTS POSITIVE)
NOT INSTABILITY-RELATED (CAPSULAR TESTS NEGATIVE)
Traumatic Instability
Atraumatic Trauma Instability Onset Insidious Onset
Rehabilitation potential limited
Good rehabilitation potential
Defined injury
Less defined process Rehabilitation potential specific to injury and process
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Apprehension Test—Anterior-Inferior Capsule. The apprehension test is performed with the patient sitting, standing, or supine. The examiner passively moves the humerus into maximal external rotation with the arm at 90 degrees abduction. The examiner may also add an anterior push to the posterior humeral head during the test as well. Lo and colleagues8 have reported a high specificity (99%) and moderate sensitivity (53%) with this maneuver to confirm anterior instability. An important discriminator for this test is to document apprehension, not pain; for example, if one places significant loading into external rotation, end-range tension is often reported as painful. Unfortunately, in my experience, examiners often report this as a positive test, which was not the original intent.9 Relocation Test—Anterior-Inferior Capsule. When the apprehension test is deemed positive, many examiners will then use the relocation test to further confirm or complement the apprehension test results. The patient is in a supine position and the examiner places one hand over the humeral head and applies a posterior force to maintain the humeral head in a posterior position. The examiner then externally rotates the humerus in the 90-degree abducted position, repeating the apprehension test, to determine whether the previous apprehension action is eliminated. Speer and associates9 have examined the relocation test in relation to surgical findings of anterior-inferior instability and found a specificity of 58% and a sensitivity of only 30%. They noted that patients often confuse pain and apprehension, greatly diminishing the actual selectivity of this and the apprehension test. Posterior Drawer Test—Posterior Capsule. The posterior drawer test is accomplished with the patient in a supine position while the examiner grasps the forearm and flexes
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the elbow approximately 120 degrees. The shoulder is then flexed approximately 90 degrees; the other hand of the examiner is placed under the scapula to enable palpation of the humeral head when a posterior force is applied through the humerus. The patient often does not have a strong reaction other than possibly sensing the humerus as slipping posteriorly. There are no specific references of the values associated with this test; many clinicians only use it if the subjective complaints of the patient indicate posterior instability. Some clinicians modify the loading process by adding a crossing of the arm over the chest to assess the actual slipping of the humeral head further. Again, no specific sensitivity/specificity data are available for this test. Capsular Assessment Interpretation Instability Related (Capsular Tests Positive). The completion of this sequence delineates the capsule as the superior (sulcus), anterior (load and shift), anterior-inferior (apprehension and relocation), and posterior (load and shift and posterior drawer) segments are evaluated. If the patient has a large sulcus, it is normally bilateral and the other tests will demonstrate significant motion as well. This is the classic multidirectional (atraumatic) instability patient who responds well to rehabilitation at a relatively high rate, a 70% or higher success rate in my experience. The patient with a positive apprehension test, not pain, has a problem usually related to a traumatic instability and has a limited response to rehabilitation. There may be the rare case of the patient who was born with a loose capsule that is then torn loose. However, these capsular tests efficiently categorize most problems as being related to instability and define the type of instability, which then helps predict rehabilitation success or failure and overall outcomes. Also, patients are often seen who have a positive instability assessment but have developed secondary problems in their attempt to live with the underlying instability. Thus, although the second portion of the shoulder screen is designed for patients without instability, we frequently have positive findings in both instability and what may be perceived as not instability tests. We sometimes describe this as having “fleas and lice.” The clinician is always urged to screen the capsule initially unless an obvious deformity prevents this. Not Instability Related (Capsular Tests Negative). The second phase of the screen is usually begun with the patient in the supine position as the process continues from the posterior drawer or apprehension test and the assessment of specific structures is initiated. (The problem has been determined not to be related to instability after completion of the capsular screen.) The acromioclavicular joint is palpated first and then tested specifically. Specific structures are now examined, with the patient’s subjective comments helping direct the flow of examination. Typically, if the patient has experienced trauma, the examination will focus on what is related to the specific force. However, when not related to trauma, the following sequence or screen pattern is efficient.
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Acromioclavicular and Labral Assessment Palpation and Crossed Arm Adduction. The patient is supine and the examiner palpates the acromioclavicular (AC) joint while the other hand passively grasps the flexed elbow and crosses the humerus across the body. The test is positive if significant pain is reported, particularly at the end range. The sensitivity has been reported to be 77%, with a specificity of 79%.10 Active Compression (O’Brien) Test. This test is done to assess AC and superior labral anterior-posterior (SLAP) lesions. The patient is standing or sitting and the examiner is at his or her side. The patient elevates the shoulder to 90 degrees (elbow extended) and then moves it (horizontal adduction) across the body to 10 to 15 degrees past midline. He or she is then asked to rotate the thumb downward; the examiner places a downward force on the humerus that the patient resists. This test is then repeated with the thumb up. Positive test results are significant pain as the patient resists the downward force. A positive test for the AC joint is pain on the top of the shoulder during both tests while a superior labral pathology is suspected if the test is only positive with the thumb down and significantly lessened when repeated with the thumb upward. The specificity of this test for labral pathology is relatively high (more than 90%) but is more limited in sensitivity (41%), with slightly higher values for AC assessments.10,11 Labral Tests Crank Test. This test is performed with the patient supine and the arm elevated in the scapular plane to approximately 160 degrees, with the elbow flexed slightly. The examiner then applies compression (axial load) through the elbow while internally and externally rotating the humerus. Pain is most common during external rotation and is often correlated with the patient complaining of pain during functional shoulder activities. Lui and coworkers5 have reported specificity and sensitivity as greater than 90%. Biceps Load I and II; Pain Provocation Tests. Several labral tests that use the biceps to bias labral loading have been reported. All these tests usually begin with the humerus in a 90-degree apprehension position, with additional pronation and supination of the forearm. Mimori and colleagues12 have reported a 100% sensitivity and a 90% specificity, whereas Kim and associates13 have reported a sensitivity of 90.9% and a specificity of 96.6% for these tests for SLAP lesions. Labral pathology is commonly the result of injury superimposed onto the labrum, allowing it to experience loads that are normally controlled by other structures. Liu and Henry14 have used this approach in evaluation of the labrum by grouping the positive load and shift test (capsular incompetency) with apprehension, relocation, sulcus, and crank tests; they reported a sensitivity of 90% and a specificity of 85%.
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At this point in the screen, we have evaluated the capsule (determined whether the problem is instabilityrelated and the type, if instability) and specific structures, the acromioclavicular joint, and labrum. The next assessment usually involves impingement signs and tests.
Impingement Testing Numerous impingement tests have been developed to elicit the pinching of tissues between the acromion and humeral head (classic external impingement). Many of these tests are plagued by being positive secondary to other conditions causing the impingement; thus, clinicians must always be wary of an easy assumption. Neer’s Sign. The patient is standing or sitting with the arm elevated overhead to the end range. The examiner forces the arm into maximal elevation, with slight overpressure. The test is considered positive with pain at the end range of motion. Some clinicians modify this examination by altering the position of the scapula to decrease pain (retraction), to increase pain (protraction), or increase pain (humeral internal rotation). Calis and colleagues15 have reported sensitivity values of 89% but a specificity of 31%. I often do the initial test in neutral humeral rotation and then repeat with internal rotation if the initial test was positive. The underlying assumption is that the second test should be more painful. The scapular position can similarly be altered but may be more difficult to control than humeral rotation, but it is also reassuring to be able to demonstrate a decrease in pain through proper positioning of the scapula to document likely rehabilitation success. Hawkin’s (Kennedy) Test. The patient is standing and the flexed arm is elevated to 90 degrees in the scapular plane. The examiner is at the patient’s side and internally rotates the humerus. A positive test is the response of pain with end-range rotation. When positive, this test can be modified by asking the patient to retract the scapula and repeat with scapular retraction being maintained. If the response is minimized, rehabilitation may include a focus on scapular or proximal musculature. Calis and associates15 have reported a sensitivity of 92% but specificity values of 25%. If this is the only positive test for impingement, the therapist should carefully evaluate the AC joint further, because a level of cross-arm adduction can occur and may be painful in those with AC pathology. Painful Arc Test. The patient is standing or seated and asked to abduct the arm actively away from the body (abduction plane) in a smooth rhythmic fashion. If the patient perceives pain in the 60- to 120-degree portion of the movement, but has pain-free movement above the painful arc, a positive test is recorded. This test can be modified to increase pain perception by adding a level of
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humeral internal rotation during the maneuver. This test was reported to have a sensitivity of 33% but a specificity of 81%.15 Rather than relying on a single test, the clinician is urged to use a combination of tests to achieve acceptable sensitivity and specificity values. By combining these three assessments, actual pathology can be more effectively determined, similar to that described previously for the labral tests by Liu and Henry.14 Just as with labral pathology, it is vital to recognize that impingement is often an accompanying diagnosis because of other causative factors.
Internal Impingement In the throwing athlete, the term internal impingement has been created to describe the condition in which the athlete reports pain at maximal external rotation associated with the throwing motion, also known as posterior impingement. The athlete is standing or seated and the arm is positioned at 90 degrees. The arm is then maximally externally rotated, and pain at the end range is considered positive if it replicates the chief complaint of what the athlete has perceived during throwing. Meister and coworkers16 have demonstrated a sensitivity of 75% and a specificity of 85% but these values were both greater than 90% if the onset was gradual and in an overhead thrower. At this point, the focus normally proceeds to individual musculotendinous structures. The reader is urged to review specific texts related to the intricacies of this process, such as Muscles: Testing and Function. Only a summary of the screening assessment will be presented here that relates to the most commonly involved muscle-tendon units in the overhead athlete.
Rotator Cuff Assessment (Primarily Supraspinatus and Infraspinatus) Integrity of the superior rotator cuff musculature is assessed through various loading techniques attempting to determine the supraspinatus and infraspinatus levels of function. Most clinicians use a combination of tests of active (movement to a position with additional resistance) and holding of a position (lag signs) to assess the function of these structures. Quantification of these tests is always a challenge because complete disruptions are often relatively easy to confirm, whereas combinations and partial disruptions are more difficult to delineate. Drop Arm Test. This classic test is designed to determine the function of the supraspinatus. The patient stands and elevates the arm to shoulder height in the scapular plane. The full can test is done with the thumb up while the empty can test is done with the thumb down. The examiner
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adds a downward force while the patient maintains the elevated position. Itoi and colleagues17 have reported that using the combination of pain and weakness yields a sensitivity of 86% and 89% with a specificity of 57% and 50%, respectively, for the full can and empty can positions. Note that the thumb down—empty can test—has a tendency of increasing pain but not improving diagnostic values. A modification that I often use is to make the patient lower the arm slowly against some downward force to assess the eccentric function of the supraspinatus. I frequently have seen this to be difficult for patients with small or possibly partial tears, which may be helpful in further reinforcing the likelihood of involvement. Significant weakness correlates highly with supraspinatus tears, particularly large tears. It is less reliable when it is more of a painful response rather than true weakness. In this case, the use of an injection to ablate pain can be helpful. I have examined a series of 25 patients with suspected involvement of the supraspinatus through the use of a posterior shoulder injection, xylocaine and corticosteroid. Isometric strength of the external rotators and abductors was measured before and after injection. If pain was ablated and strength increased, impingement is indicated, whereas ablation of pain but no resulting increase in strength indicates rotator cuff tear. Resisted External Rotation. The patient is seated with the arm in neutral position while the elbow is typically flexed 90 degrees. The examiner applies a force in the direction of internal rotation and the patient is asked to resist the force. The examiner compares right with left for determination of the normal. Significant weakness provides good sensitivity (more than 90%) but lower specificity (75%).18 Lag Signs of the Rotator Cuff. The use of positioning that requires stabilization against gravity is useful to elicit the lack of function of the cuff musculature. European researchers have used the hornblower’s sign (positioning of the arm to allow blowing of a horn) and maintaining external rotation while elevating the arm in the scapular plane to delineate this process; U.S. researchers refer to this as the lag sign. The most common sequence used is positioning the arm in the scapular plane and then passively positioning the humerus into external rotation maximally and asking the patient to maintain the rotation. Some examiners prefer to do this at 20 to 30 degrees of scapular abduction and others prefer higher levels of abduction. If higher abduction is used, the examiner must provide support under the elbow because supraspinatus involvement will preclude appropriate external rotation assessment when a significant tear of the supraspinatus is present. Hertel and colleagues19 have quantified the amount of drop and showed that if more than 10 degrees of drop is seen, patients are found to have combined tears of the
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supraspinatus and infraspinatus. These lag tests can thus have high sensitivities when significantly positive (more than 90%). Multiple variations of the tests are commonly described in textbooks and articles. The clinician is urged to read with a critical eye and apply a battery of tests whenever possible to better define pathology. Rehabilitation success is related to the actual structural involvement. Consequently, the better the evaluation, the greater the opportunity for predicting the nature of required care. I often proceed with strength and functional assessments after completion of the screen in the athlete, because dynamic function requires the synchronous interactions of active and passive elements, which are not assessed through traditional orthopedic examination and screening.
Strength Assessment Our assessment of muscular output is typically performed noninvasively. Thus, although muscle tissue is generating tension through its attachments by tendon to the skeletal system, the absolute tension-generating capacity of the muscle is not measured. Instead, changes in multiple components of the ability of the muscle to generate tension and alterations in the skeletal system, and corresponding changes in length-tension ratios, rotational orientation, compression, leverage, and angulation, are assessed.20,21 The operational definition of strength is delineated by the assessment methodology, which determines whether force, torque, power, and/or work values are measured. Some have recommended isometric assessment as the most appropriate method to minimize some of the alterations described earlier.22 The shoulder is a dynamic joint, because it completely depends on musculature for its stability and functional patterns. Although fraught with dangers, combining isometric assessment of individual muscle functions with dynamic assessment of movement patterns provides a clearer understanding of the tissues involved and appropriate intervention.
MUSCLE ACTIONS Characteristics of muscle action are presented in Table 3-2. The assessment of muscle action is best described as muscle activation, with the external load determining the observed function. This means that an object will be lowered with control, held in place, or raised by the applied muscular action. This obviates the problem of describing an eccentric activity as a muscle contraction when actually the muscle fibers are controllably lengthening. It is important for the clinician to determine whether the patient is describing difficulties with concentric or eccentric actions, because the inherent stability and functioning of the
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TABLE 3-2 Characteristics of Muscle Actions Type
Action
Level of Output/Unit Area Metabolic Demands
Isometric
Tension-producing, no motion
Moderate
Intensity-related
Isotonic
Movement of a resistance (weight) through a range of motion
Low/moderate
High
Isokinetic
Machine-controlled speed of motion
Low/moderate
High
Isotonic
Weight being lowered through a range of motion
Low
Low
Isokinetic
Machine-controlled speed of motion “driving” the muscle to a length while activated
High
Low (?) (best guess)
Concentric
Eccentric
shoulder complex require a controlled sequence of all three types of muscle activity or activation.
validity25 but, again, prevent assessment of the dynamic shoulder.
In general terms, eccentric contractions generate the highest tension per unit area of muscle, followed by isometric and concentric actions. Isometric assessment or action may be the best opportunity to assess tension capability of the active component of the musculature but may be of limited value in predicting functional capacity. Concentric actions can be performed isotonically or isokinetically but are frequently misinterpreted because of the inhibitory effects of effusion, pain, and altered recruitment.21,23
Cable Tensiometry. Cable tensiometers assess isometric output through a perpendicular tension assessment developed by Clarke.26 These devices have not gained wide acceptance in clinical settings and have been used primarily in a testing situation; they are generally not used for function or rehabilitation of patients.
Isometric Techniques Manual Muscle Testing Manual muscle testing is a frequently used system of manually applying loads against gravity or with gravity minimized to determine the voluntary response of the patient. Patients must be urged to be consistent in how they assess (make or break) and in their position of evaluation (midrange or locked) to minimize differing results.24 Problems of manual muscle testing include assessment of athletes who surpass normal and the tremendous difficulty in intertester reliability. The length of time allowed to generate tension and the ability to reproduce this on a repeated basis, coupled with the problems of multijoint muscle assessment, make manual muscle testing useful for screening patients but of limited value in attempting to assess muscular output objectively in the dynamic shoulder. Hand-Held Dynamometry. A number of hand-held dynamometers have been developed to enhance the objectivity of a manual examination. These devices have been shown to be acceptable clinically in terms of reliability and
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Isotonic Assessment Isotonic weight lifting involves the movement of a weight through a range of motion in raising (concentric) and lowering (eccentric). Problems include limitations by the neural drive through the central nervous system and inhibitions that may occur through the peripheral system. This includes the person’s ability to recruit muscle and his or her ability to use it in different formats, including concentric and eccentric patterns. This leads to the difficulty of endurance and repeatability of actions. The isotonic movement is limited to the weakest link, which is typically the maximal concentric pattern, such as 90 degrees of abduction at the glenohumeral joint. Factors vital to isotonic assessment include lever arm length and speed of movement. The perpendicular distance from the axis of rotation dictates the force required for the movement, whereas the person’s ability to move quickly and smoothly provides much information about the functional capability of the dynamic shoulder. A stronger individual can accelerate a particular weight in a freer and more controlled pattern than a weaker individual; however, this also requires looking closely at substitution and requirement of synchronous action before automatically accepting the performance of the stronger individual as being adequate. Inherent in the isotonic assessment are fatigue and completion of range of motion during testing.
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Isotonic measurements may reflect function, particularly in activities that require fairly slow movements. However, the average speed of isotonic assessment is approximately 60 deg/sec, and concentric assessment may not reflect eccentric performance.21,22,27 Clinicians will continue to use isotonic assessment but should recognize that it primarily reflects concentric performance unless additional loading is provided during assessment. I recommend this, particularly when assessing the supraspinatus and external rotators, because these are often functioning in an eccentric, stabilizing, and reducing pattern.
Isokinetic Assessment
51
must be determined. Assessment of strength is a multifaceted problem caused by the inability to take direct measurements and by the effects of such factors as neural drive, inhibition, pain, or changing lever arms. Although the ability to measure output has improved substantially, techniques directly related to function have not been developed. Because the shoulder joint is dynamic, caution must be exercised when interpreting muscular assessment results. Clinicians are urged not to overinterpret and use single pieces of data that are often provided by isokinetic devices.
FUNCTIONAL ASSESSMENT
Isokinetic exercise devices involve speed-controlled movements as the patient accelerates a lever arm to a predetermined maximal velocity and then moves through a range of motion and decelerates at the end of the range to the terminal position.28,29 One of the primary advantages of this type of assessment is the ability to evaluate individual muscle patterns in a dynamic orientation while providing some inherent stability to the testing positions. The information collected from these machines is in a machinespecific format; different machines handle the collected data through different software programs.30
Performance evaluation is a critical part of the evaluation schema. It is not unusual for no problem to be determined through clinical evaluation until more detailed information about dynamic shoulder function is obtained. This is why many practitioners now use the term clinical stability rather than functional stability. Functional stability requires neuromuscular integration and synchronous activity to enable the performance of high-demand dynamic movements.
Another use of isokinetics involves the evaluation of eccentric actions. Isokinetic (speed-controlled) eccentric actions can be performed two ways—by overcoming a predetermined load and having the lever arm drive the extremity at the predetermined velocity, or by having the individual work against a passively moving lever arm at the predetermined velocity. The neurophysiology of these actions may be different from the eccentric activity seen with isotonic actions, and again these actions are machinespecific in their interpretation. There is a different pattern of torque production with isokinetic concentric activity decreasing as speed increases compared with a relative plateau seen with eccentric peak torque assessment.21
The evaluation of performance should be directed toward the activities required of work or desired athletic pursuit, which is generally why the patient has come for evaluation. Thus, the evaluation of function should be patient specific. As noted, the clinician must attempt to determine not only the location of pain but also the actions of structures at that point in the functional pattern. Concentric pain usually indicates musculotendinous junction problems or impingement of bony, labral, or soft tissues. Eccentric pain is typically related to tendinous lesions or high-demand decelerative efforts to provide dynamic stability. Although this sounds fairly simplistic, the interpretation of functional activities can be extremely difficult and challenging for experienced as well as inexperienced clinicians.
Although clinicians have grown accustomed to the interpretation of isokinetic exercise being performance oriented, minimally true patterns of function or performance are being evaluated. The limitations of isokinetic assessment with open and closed kinetic patterns and with functional levels in speed being somewhat inconsistent must be recognized. For isokinetic assessment to have meaning, a standardized protocol for the evaluation should be followed.31 Evaluation via isokinetics should be accomplished only after the clinician has determined what he or she wishes to evaluate and the type of contraction that would be most appropriate, enabling meaningful information to be obtained. Thus, which plane of motion to evaluate and which would be the most appropriate testing position
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CONCLUSIONS The difficulty of assessing these components, which function in a dynamic pattern about this soft tissue structure, must be recognized. Shoulder evaluation must be systematic and activity specific. I recommend the use of a systematic screen that initially clears the capsule before specific structures are examined. As noted, not all problems are related to a single structure, which leads to difficulty in isolating pathology and best establishing the treatment sequence. Clinicians have a tendency to apply a single protocol of treatment that may not address all patterns or involved structures. The following case study exemplifies this problem.
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CASE STUDY A 15-year-old female swimmer with a 6-month history of bilateral shoulder pain (right greater than left) presented to our clinic with the previous diagnosis of impingement. Her treatment had included strengthening (internal rotators and external rotators), anti-inflammatories, and rest. Continued problems led her to receive bilateral corticosteroid injections with minimal response. Her radiographs had been negative and she had just been told that it is common for swimmers in her age group to continue to have such problems. We observed a healthy 15-year-old swimmer whose right shoulder was visibly lower than the left, as was the scapular position, with the right demonstrating a somewhat more protracted rest position; she had forward head posture and a very strong bilateral internal rotation bias. Her present swimming routine involved 3000 to 5000 meters in the morning followed by 3000 to 5000 meters in the afternoon, with most of these strokes being freestyle. Her routine had included the use of hand paddles during the past 6 to 8 months, when she also developed her impingement problems. Range-of-motion evaluations, both active and passive, revealed an internal rotation limitation of approximately 10 degrees bilaterally, but she moved her scapulae and trunk to achieve the additional movement. Her instability assessment revealed a positive posterior apprehension test on the right, as well as a similar apprehension relation on the right. She had some posterior labral tenderness on the right during testing and also exhibited positive impingement bilaterally.
STRENGTH ASSESSMENT Her manual muscle test revealed weak external rotators with very strong internal rotators. Her isokinetic assessment (prone data) revealed a 42% external rotation–to–internal rotation ratio.
FUNCTIONAL ASSESSMENT Her activities obviously revolved around swimming and her associated training techniques. She had been doing a strengthening routine but continued to emphasize internal rotators rather than attempting to correct the imbalance with her external rotators. It was important when testing her to do the testing in a prone position to duplicate her functional positions. Our assessment led to the recognition that she does have impingement, but it is secondary to lack of humeral head
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control associated with instability. She also has an activityrelated problem with swimming, particularly with emphasis on the use of hand paddles. As her external rotation strength was enhanced and her use of hand paddles eliminated, her symptoms began to resolve rapidly. She became essentially asymptomatic when a 50% external rotation–to–internal rotation ratio was achieved. Frequently, a person who has some instability and impingement overlap may do fairly well if dynamic control is enhanced. As with most clinical activities, evaluation is the key. Proper rehabilitation and interventions can be provided only when the specific structure is enhanced within an overall context. The goal of the clinical examination must be to establish the nature and severity of the injury or pathology and dysfunction, and to address these most appropriately.
References 1. Andrews JR, Gillogly S: Physical examination of the shoulder in throwing athletes. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, pp 51-65. 2. Cyriax J: Textbook of Orthopaedic Medicine, 8th ed. Philadelphia, Bailliere Tindall, 1982. 3. Hoppenfeld S: Physical Examination of the Spine and Extremities. East Norwalk, Conn, Appleton-Century-Crofts, 1976. 4. Magee DJ: Orthopaedic Physical Assessment. 4th ed. Philadelphia, WB Saunders, 2002. 5. Liu SH, Henry MH, Shapiro MS, et al: Diagnosis of glenoid labral tears: A comparison between magnetic resonance imaging and clinical examinations. Am J Sports Med 24: 149-154, 1996. 6. Hawkins RJ, Schutte JP: The assessment of glenohumeral translation using manual and fluoroscopic techniques. Orthop Trans 12:727-728, 1988. 7. Neer CS, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980. 8. Lo IK, Nonweiler B, Woolfrey M, et al: An evaluation of the apprehension, relocation, and surprise tests for anterior shoulder instability. Am J Sports Med 32:301-307, 2004. 9. Speer KP, Hannafin JA, Altchek DW, et al.: An evaluation of the shoulder relocation test. Am J Sports Med 22:177-183, 1994. 10. Chronopoulos E, Kim TK, Park HB: Diagnostic value of physical tests for isolated chronic acromioclavicular lesions. Am J Sports Med 32:655-661, 2004. 11. O’Brien S, Pagnani M: The active compression test: A new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med 26:610-613, 1998. 12. Mimori K, Muneta T, Nakagawa T, et al: A new pain provocation test for superior labral tears of the shoulder. Am J Sports Med 27:137-142, 1999.
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13. Kim SH, Ha KI, Ahn JH, et al: Biceps load test. II: A clinical test for SLAP lesions of the shoulder. Arthroscopy 17:160164, 2001. 14. Liu S, Henry M: A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med 24:721-725, 1996. 15. Calis M, Akgun K, Birtane M, et al: Diagnostic values of clinical diagnostic tests in subacromial impingement syndrome. Ann Rheum Dis 59:44-47, 2000. 16. Meister K, Buckley B, Batts J: The posterior impingement sign: diagnosis of rotator cuff and posterior labral tears secondary to internal impingement in overhead athletes. Am J Orthop 33:412-415, 2004. 17. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test” in detecting the torn supraspinatus tendon? Am J Sports Med 27:65-68, 1999. 18. Lyons A, Tomlinson J: Clinical diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 74:414-415, 1992. 19. Hertel R, Ballmer FT, Lombert SM, et al: Lag signs in the diagnosis of the rotator cuff rupture. J Shoulder Elbow Surg 5: 307-313, 1996. 20. Williams M, Lissner HR: Biomechanics of Human Movement. Philadelphia, WB Saunders, 1966. 21. Malone TR: Muscle injury and rehabilitation. In Sports Injury Management, vol 1, no. 3. Baltimore, Williams & Wilkins, 1988, pp 43-74.
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22. Rothstein JM: Measurement in Physical Therapy. New York, Churchill Livingstone, 1985. 23. DeAndrade J, Grant C: Joint distension and reflex inhibition in the knee. J Bone Joint Surg 47:313-322, 1965. 24. Poland J, Hobart D, Payton O: The Musculoskeletal System. Garden City, NY, Medical Examination Publishers, 1981. 25. Bohannon R: Test-retest reliability of hand-held dynamometry during a single session of strength assessment. Phys Ther 66:206-209, 1986. 26. Clarke HH: Cable Tension Strength Test: A Manual. Springfield, Mass, Stuart E. Murphy, 1953. 27. Sanders M, Sanders B: Mobility: Active-resistive training. In Gould J, Davies G (eds): Orthopaedic and Sports Physical Therapy. St. Louis, Mosby, 1985, pp 228-241. 28. Davies G: A Compendium of Isokinetics in Clinical Usage, 2nd ed. LaCrosse, Wis, S&S Publishers, 1985. 29. Lesmes GR, Costill DL, Coyle EF, Fink WJ: Muscle strength and power change during maximal isokinetic training. Med Sci Sports 10:266-269, 1978. 30. Malone TR: Evaluation of isokinetic equipment. In Sports Injury Management, vol 1, no. 1. Baltimore, Williams & Wilkins, 1988, pp 1-90. 31. Wilk KE, Arrigo CA, Andrews JR: Standardized isokinetic testing protocol for the throwing shoulder: The throwers’ series. Isokin Exerc Sci 1:63-71, 1991.
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CHAPTER 4 Clinical Examination of the
Shoulder Complex Michael J. Kissenberth, James F. Silliman, and Richard J. Hawkins
An accurate and thorough examination can only be performed in a relaxed environment. The patient should be clothed so that he or she is relaxed, but the examiner should have adequate visibility of both shoulder girdles and the upper trunk. The examination is performed with the patient standing, sitting, supine, or prone, as necessary. The history often influences the clinician to focus on a specific aspect of the examination, but an organized screening examination should be performed on every patient. Because of the interaction of the many factors contributing to the symptom complex in these athletes, it is essential to have a thorough understanding of the entire shoulder girdle, especially the glenohumeral and scapulothoracic interplay. The athlete’s shoulder creates many diagnostic dilemmas because of the fine balance between extreme mobility and instability.
Successful management of any clinical problem begins with an accurate history and physical examination. This chapter will describe physical examination of the athlete’s shoulder. Overhead athletes who swim, throw, and serve present with special problems. The extreme forces that act on the shoulder girdle during these activities cannot be re-created in a typical examination. With new technology for assessment, such as motion analysis, we now know that these forces often exceed the physiologic limits of the capsuloligamentous restraints of the rotator cuff.1 If the rate of injury (overuse) exceeds that of repair, impairment and dysfunction result.2 As we have advanced in our understanding of the throwing shoulder, we also see loss of internal rotation and posterior capsular tightness as an early manifesting symptom. Pain is often the most common manifesting symptom.3 The emphasis on the cause of this pain has evolved from biceps3,4 and rotator cuff impingement tendinitis5-9 to anterior instability and posterior capsular tightness, with obvious overlap among these causes in many athletes.
We suggest an organized, thorough, and consistent format when examining an athlete’s shoulder. Re-creation of the patient’s symptoms with certain maneuvers may help the examiner arrive at an accurate diagnosis. Great variability exists from patient to patient in regard to range of motion, joint laxity, and strength. Often, certain sports require emphasis on different aspects of these facets. For example, gymnastics demands hypermobile or hyperlax joints, and weightlifting demands excess strength. Often, the final question before beginning the examination is to ask the patient to point with one finger and touch the area where the problem is located. The examination proceeds in the following sequence, remembering that presentation can be in the acute setting immediately after an injury or, more often, in a chronic situation presenting to the clinic or office.
Prior to beginning the clinical examination, it is imperative to obtain a chief complaint, an accurate history, and a full understanding of the athlete’s sport, level of participation, position played, motivation, and expectations. For example, a baseball pitcher who has thrown many pitches may have tendinosis, labral tears, or subtle anterior instability. A football player who falls and has a traumatic injury may have dislocated the shoulder or fractured the clavicle. A thorough understanding of the initial event or injury is helpful in the initial development of a differential diagnosis. Communication with the family and athletic trainer is also helpful in obtaining additional objective information and feedback regarding the athlete and the injury. It is essential to ask the patient if he or she has had any prior treatment to include periods of rest, injection, physical therapy, and medication. The location and response to the injection can provide valuable information before beginning the examination. Often, the athlete arrives with a magnetic imaging resonance (MRI) scan and a presumptive diagnosis based on the MRI reading. Although this is often helpful information, the MRI scan can often lead the physician down the wrong path and should not influence the initial examination. We recommend waiting to review the MRI scan until after the history and examination have been completed.
INITIAL EVALUATION Cursory Impression On first visualizing the athlete, an initial cursory impression encompassing many factors is formed. For example, a large muscular individual with a mesomorph frame obviously suggests someone in a strength-type of sport, such as weightlifting or football. A petite young woman might well suggest involvement in gymnastics. In analyzing these patients, we may see those who have an acute injury presenting with significant pain, which influences our approach to the situation. The older athlete presenting to the office in a business suit presents a different impression 55
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than the 6-foot 10-inch basketball player who walks into the athletic clinic directly from practice.
Inspection Inspection should be performed from different perspectives— that is, from the front, side, back, and top—noting attitude (symmetry), muscles (wasting or hypertrophy), deformities (e.g., scars, lumps, bumps), any evidence of discoloration such as bruising and swelling. The way the athlete carries the upper trunk and shoulders provides clues as to the diagnosis. For example, an athlete with a painful shoulder may show asymmetry between the trapezius contours when looking from the front and back. Dominance may lead to asymmetry between the sizes and contours of the different shoulder girdle muscles. The symmetry of the borders of the clavicle, acromioclavicular joint, and sternoclavicular joints should also be noted. Deformities in these areas are often revealing. Scars should be inspected, not only as evidence of previous surgical procedures, but also for widening or spreading of the scars, which may denote a collagen abnormality, as seen in patients with multidirectional instability.10 Evidence of wasting of different muscles or muscle groups may suggest certain diagnoses. Deltoid wasting may appear as prominence and squaring of the acromial borders. Supraspinatus and infraspinatus wasting can be related to rotator cuff tear11 or, rarely, to suprascapular nerve injury (Fig. 4-1).12 In particular, infraspinatus atrophy is often a sign of a large rotator cuff tear in an older patient; however, in a throwing athlete, a cyst in the spinoglenoid notch causing compression on the suprascapular nerve must be considered.13 Occasionally, hypertrophy of a muscle such as the trapezius may be caused by muscle spasm. A patient with a recent injury may have bruising, with associated discoloration. Swelling and discoloration are uncommon in chronic complaints but often manifest with acute trauma.
Figure 4-1. Supraspinatus and infraspinatus atrophy. Atrophy is caused by compression of the suprascapular nerve.
From behind the standing patient, the scapulothoracic joint with forward flexion and abduction is observed. Scapular winging can be demonstrated by asking the patient to elevate the arms forward at about half speed, with maximum winging usually demonstrated by applying resistance at about 30 degrees of forward elevation. The patient can also be asked to perform a wall push-up (Fig. 4-2). Ligamentous laxity can be observed with extension of the elbow or a thumb-to-forearm examination (Fig. 4-3).
Observation Before focusing on range of motion about the shoulder, it is helpful to appreciate glenohumeral and scapulothoracic synchrony. Beginning at 30 degrees of abduction, every 30 degrees of glenohumeral abduction relate to 12 degrees of scapular rotation.14-16 Dyskinesia or asynchrony of this coupled mechanism can be related to loss of range of motion or guarding. Weakness of the scapular stabilizers with resultant scapular winging can be part of the symptom complex of anterior shoulder pain, especially in the throwing athlete. It is common for the throwing athlete or patients with subtle forms of multidirectional and posterior instability to have scapular winging. This is usually not related to a neurologic deficit but rather to dyskinesia of the scapulothoracic articulation.
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Figure 4-2. Scapular winging. Winging is present bilaterally by applying resistance at 30 degrees of forward elevation.
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A
Palpation As noted, it is helpful to ask the patient to point with one finger and touch the area of maximum tenderness. Thorough palpation of the shoulder girdle is now performed, noting warmth, tenderness, deformity, and crepitus. It is often helpful, as confidence of the patient is gained, to wait and palpate the area of maximum tenderness at the end of this part of the examination. Starting from the back, palpation of the cervical spinous processes, scapular spine, medial border of the scapula, and scapular angle may reveal tender areas. Scapulothoracic bursitis at the inferior medial angle of the scapula may manifest in baseball pitchers.17,18 Superior angle tenderness and snapping in the tennis serve are common manifesting complaints. The posterior cuff and joint capsule should be palpated deep to the infraspinatus muscle belly. The posterior cuff is often tender, not only with posterior instability but also with internal impingement.13 Posterior capsular ossification can lead to significant pain and dysfunction during the throwing motion.19 Palpation of the rhomboids, latissimus, supraspinatus, and infraspinatus can provide an assessment of their tone. Palpation of the quadrilateral space below the posterior joint is an important area to localize and palpate, especially in overhead athletes, because of possible compression of the neurovascular structures when the arm is in maximum abduction and external rotation, the cocking position.20 The quadrilateral space is bordered by the teres minor superiorly, the teres major inferiorly, the humerus laterally, and the long head of the triceps medially. Clinical findings include vague pain and paresthesias around the shoulder and pinpoint tenderness at the quadrilateral space. From the back, the location of the bicipital tendons can be palpated simultaneously to ascertain tenderness (Fig. 4-4).
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B
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Figure 4-3. Ligamentous laxity and hypermobility. These can be appreciated from observing the patient’s hyperextensible elbows (A) or the thumb-to-forearm examination (B).
The clinician can locate the bicipital groove by directing his or her fingers anteriorly and distally to the acromioclavicular joint, with the patient’s arm in approximately 10 degrees of internal rotation. Moving to the front of the standing or seated patient and palpating the sternoclavicular joint statically, and with arm rotation, may reveal tenderness, crepitus, or even instability. The clavicle and acromioclavicular joint are also palpated in this way. It is important to palpate the acromion and not to forget about the symptomatic os acromiale. A common injury in the collision athlete, especially in football, is to the acromioclavicular joint.21 Acutely, athletes can present with a wide range of severity of injury and deformity to this joint, with varying degrees of
Figure 4-4. Bicipital groove palpation. Palpating both grooves at the same time serves as a good comparison examination for tenderness.
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prominence of the outer clavicle. The classification scheme of Rockwood and Green22 is useful for appropriate management. Chronic injury to the acromioclavicular joint can lead to hypertrophy, pain, instability, and degenerative joint disease. A symptomatic acromioclavicular (AC) joint is often tender to palpation and the cross-arm adduction test is used as a provocative maneuver to elicit pain at this joint.23 The arm is forcibly adducted across the chest wall, producing pain on top of the shoulder (Fig. 4-5). This test can be positive with labral tears and with cuff pathology, so it is important to have the patient indicate where this test causes pain. Pain felt deep in the shoulder may occur because of a superior labral anterior-posterior (SLAP) tear (see later). The Paxinos test can also help diagnose AC joint pathology. This is accomplished by compressing the AC joint with the index finger anterior to the clavicle and the thumb on the posterior edge of the acromion.24 Injection of 5 mL of 1% lidocaine directly into the joint, with relief of the symptomatology in the cross-arm test, can assist in the diagnosis of primary acromioclavicular pathology. The subacromial arch is assessed initially with palpation of the greater tuberosity and supraspinatus insertion (Codman’s point). With circumduction of the arm, an appreciation of the crepitus is important, especially in rotator cuff disease and degenerative joint disease of the glenohumeral joint. A positive clunk test or labral grinding can suggest labral pathology.25 Palpable crepitus or grinding, with the arm abducted to 90 degrees and the humeral head translated to the anterior rim of the glenoid with a
Figure 4-5. Cross-body adduction test for acromioclavicular joint pathology.
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posterior force (prone or seated), and rotation of the arm, is considered positive (Fig. 4-6). Attention to the contralateral shoulder is also important and useful in palpating painful areas to use as a comparison and to validate clinical findings. There will likely be physiologic adaptations to the throwing shoulder in regards to muscle girth and range of motion (excessive external rotation) that must be taken into account during the examination.
Range-of-Motion Assessment The rhythm and synchrony of scapulothoracic and glenohumeral motion have been discussed. Athletes are often selectively or generally hypermobile in performing their different movements. For example, accomplished baseball pitchers sometimes show extremes of external rotation at the expense of internal rotation.18 However, the total arc of rotation (external rotation plus internal rotation) usually remains similar to that of the contralateral shoulder (Fig. 4-7). Pathology and glenohumeral internal rotation deficit (GIRD) may exist if the total arc of motion is 25 degrees less than that of the contralateral shoulder (Fig. 4-8).13 A pitcher will usually have excessive external rotation and a concomitant loss of internal rotation. As long as the total arc of motion is similar to that of the contralateral shoulder, an internal rotation deficit does not exist. The quality of the examination is often improved
Figure 4-6. Crank test. This test is performed by placing the abducted arm to 90 degrees, translating the humeral head anteriorly by posterior force, and palpating and feeling for crepitus, or grinding, on the anterior rim of the glenoid.
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A
59
B
Figure 4-7. Total arc of motion. A, Maximum external rotation. B, Maximum internal rotation. With the patient in the supine position, with the shoulder abducted to 90 degrees, maximum external and internal rotation are recorded. The scapula is stabilized. The other shoulder is compared and a difference of more than 25 degrees can be a sign of a glenohumeral internal rotation deficit (GIRD).
by using a worksheet to record range of motion. Examination for different ranges in different circumstances can be performed with the patient standing, sitting, or supine, depending on clinician preference. From behind the standing patient, active forward elevation is observed. The patient is allowed to flex his or her arm in the plane that is most comfortable, usually somewhere between the sagittal and scapular planes, and with the thumbs pointing upward (Fig. 4-9). Once the patient has achieved maximum active range, passive range is assessed by stressing the arm into forward elevation. This represents the classic impingement sign (see later). The passive range is recorded bilaterally in degrees. External rotation is evaluated with the arm at the side and at 90 degrees of abduction in much the same manner. Internal rotation is measured by determining where the abducted thumb reaches in reference to spinal vertebrae (Fig. 4-10). These four motions—forward elevation, external rotation at neutral and 90 degrees, and internal rotation—should be the motions selected for documentation in the athlete, according
A
to the American Shoulder and Elbow Surgeons (ASES). Strength assessment is described in the next section, but it is determined as range-of-motion testing is performed.
Strength Assessment Strength is easy to assess from behind the standing or sitting patient and can be performed in concert with rangeof-motion assessment. Unfortunately, the presence of pain may preclude a reliable assessment of strength. The routine strengths to be assessed in the athlete’s shoulder consist of forward elevation, external rotation, internal rotation, and abduction. Strength assessment is performed while testing and comparing the opposite normal side. As with all muscle testing, the muscle being tested should be given the mechanical advantage. All muscle testing should be graded using the 0 to 5 rating system (Table 4-1). Forward elevation strength (anterior deltoid) is assessed with resistance applied to the forward-flexed arm at approximately 70 to 80 degrees. External rotation strength
B
Figure 4-8. Arc of motion. A, Maximum external rotation. B, Maximum internal rotation. Note the increased external rotation that is usually seen in a thrower and the internal rotation deficit that may be present.
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A
Figure 4-9. Forward elevation.
assesses the strength of the rotator cuff, which contributes 30 to 40 degrees of the power of elevation and 80% to 90% of the power of external rotation.26 Abduction strength is also assessed in the coronal plane, and weakness may be suggestive of deltoid or cuff deficiency. At this point in the examination, there is some confluence of testing, because strength tests become part of the special diagnostic tests used to determine rotator cuff pathology, instability, and overuse throwing conditions. Therefore, specific shoulder muscle tests will be described later in this chapter.
IMPINGEMENT AND ROTATOR CUFF PATHOLOGY Impingement syndrome and rotator cuff pathology are common conditions affecting the overhead athlete and can frequently result in pain, weakness, instability, or a combination of symptoms. Pain in rotator cuff pathology often involves night pain and difficulty lying on the affected extremity. After completing the initial part of the examination, specific tests can be used to evaluate the integrity of the rotator cuff musculotendinous structures. The three impingement signs are assessed in forced elevation, forced internal rotation, and the classic painful arc. From the front of the seated or standing patient, passively stressed maximum forward elevation, which elicits pain as the rotator cuff opposes the anterior acromial arch, is the classic Neer’s impingement sign (Fig. 4-11).6,8 The Hawkins sign is elicited by placing the arm in 90 degrees of forward flexion, with the elbow flexed to 90 degrees. Pain with
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B Figure 4-10. Active rotation. A, Active external rotation. B, Active internal rotation.
forced internal rotation of the arm can be provoked by opposing the rotator cuff on the acromion and coracoacromial ligament; this is another impingement sign (Fig. 4-12).5,27 A painful arc in the abducted position in the coronal plane is also an impingement sign. This pain is often increased with resistance and by placing the arm posterior to the plane of TABLE 4-1 Rating System for Muscle Testing Grade
Descriptive Term
0, zero
Nothing
1, trace
Trace
2, poor
Gravity eliminated
3, fair
Against gravity
4, good
Near-normal
5, excellent
Normal
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Figure 4-13. Painful arc sign for impingement. Figure 4-11. Neer’s impingement sign.
signs of impingement.3 These signs are 88% to 92% sensitive, but are all somewhat nonspecific. The yield from the impingement sign is improved by evaluation of an injection test. The subacromial space is injected with 10 mL of 1% lidocaine, and the impingement tests are repeated. Abatement of pain postinjection suggests subacromial pathology.28 It is important to document the percentage of improvement after any injection because it is a prognostic indicator for surgery and provides helpful information at follow-up visits.
Figure 4-12. Hawkins’ sign.
the scapula in the coronal plane (Fig. 4-13). The stressed cross-arm adduction test can be performed and is suggestive of acromioclavicular pathology, as described earlier. Traumatic osteolysis of the distal clavicle seen in weightlifters can manifest with this positive sign, and frequently with
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The following tests can evaluate the strength and integrity of the rotator cuff. They involve standard strength testing of the specific muscles and lag tests to demonstrate weak musculotendinous units. The supraspinatus test, as described by Jobe and Jobe,17 isolates and assesses the strength of the supraspinatus tendon (Fig. 4-14). The strength of elevation is assessed at 90 degrees of forward flexion in the scapular plane, with the thumbs pointed to the floor. Downward pressure is resisted by the patient.17,29 This test is supposedly specific for evaluation of the supraspinatus function and reasonably accurate for assessment of rotator cuff strength and integrity. Unfortunately, many patients have pain, precluding the reliability of such a test. Because this test can be painful, the full can test has been described as an alternative. The thumbs are pointed up and the test is repeated as described for the Jobe test (Fig. 4-15). Resisted external rotation is then performed with the elbows flexed at the sides to assess the strength of the infraspinatus
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Figure 4-14. Jobe test for supraspinatus function.
tendon (Fig. 4-16). As with all strength tests, the normal shoulder is used as a comparison, and asymmetrical strength is documented and considered a significant finding. An external rotation lag test is used to demonstrate weakness of the infraspinatus and, when positive, is indicative of a significant tear in the musculotendinous unit. This test is accomplished by placing the patient’s shoulder at the side in neutral abduction and externally rotating the forearm; the patient then is asked to hold that position.30,31 With a fullthickness rotator cuff tear or dysfunction involving the supraspinatus and infraspinatus, the forearm will spontaneously rotate back to neutral. This test can also be performed with the shoulder in 90 degrees of elevation in the scapular plane, with the elbow flexed to 90 degrees; this is called a drop sign. The patient is then asked to maintain this position. The sign is positive if a lag or drop occurs.
Figure 4-16. External rotation (infraspinatus) motor testing.
Gerber has popularized the liftoff test to evaluate subscapularis strength and integrity. The patient is asked to lift the back of his or her hand away from the lumbar spine; this may suggest an intact subscapularis (Fig. 4-17). If performed properly, this test is reliable to identify a subscapularis
Figure 4-15. Supraspinatus thumbs up test.
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Figure 4-17. Liftoff test for subscapularis integrity.
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rupture; however, the patient will often recruit the triceps, which can lead to a false-negative test result. Technique is critical; it is necessary for the patient to keep the upper arm relaxed while performing the test. There are several variations. The same liftoff test can be performed like a lag test (internal rotation lag sign) by positioning the patient’s hand away from the small of the back and then asking the patient to hold that position. If the hand spontaneously returns to the small of the back, it is highly suggestive of subscapularis dysfunction (Fig. 4-18). The belly press test has been described as an alternative to the liftoff test, especially for patients with internal rotation contractures.20 This test is performed by having the patient place both hands on the upper abdomen and attempting to keep the arm in maximum internal rotation, with and without resistance. With a normal subscapularis, the elbow stays anterior and does not drop backward (Fig. 4-19). Both these tests have been validated for the determination of subscapularis integrity and should be parts of all shoulder examinations.
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A
BICEPS AND SLAP CONDITIONS Much attention has been given to the biceps and superior labral structures in the throwing athlete recently. There is often a mixed picture, with positive SLAP and biceps findings in patients with rotator cuff problems and those with instability. Therefore, we will describe the tests for extraarticular biceps involvement and intra-articular SLAP tears separately—these tests are performed as part of a comprehensive shoulder examination. Biceps tendon involvement
B Figure 4-19. Belly press test for subscapularis integrity. A, Intact subscapularis. B, Deficient subscapularis. Electromyographic studies have shown that this is a better test for the upper subscapularis tendon.
may be evaluated with the tests of Speed and Yergason.29 Speed’s test is performed with the shoulder in forward flexion, elbow extended, and hand supinated with applied resistance (Fig. 4-20). Pain in this position from the area of the bicipital groove is a positive finding suggestive of bicipital tendinitis.32 Resisted supination with the elbow flexed to 90 degrees is Yergason’s test.8 Once again, pain in the bicipital region with this maneuver is considered positive for biceps tendon involvement (Fig. 4-21). These are not strength tests and, if positive, are suggestive of extra-articular biceps involvement. An arthroscopic analysis of the Speed’s test has shown a specificity of 14% and a sensitivity of 90%.33 Figure 4-18. Internal rotation lag test. This is a modification of the liftoff test.
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SLAP lesions have been discussed by Snyder and associates34 and several tests were described in an attempt to
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diagnose tears to the superior labrum on physical examination accurately. As noted, much attention has been given to SLAP tears in baseball pitchers and to understanding the disabled throwing shoulder. Burkhart and colleagues13 have advanced our understanding of SLAP tears; they hypothesized that posterior capsular contracture initiates the cascade of events that eventually lead to a positive peel back of the posterior superior labrum in the late cocking phase of throwing. It is important to evaluate the arc of rotation and loss if internal rotation closely in any thrower, especially those presenting with signs and symptoms of a SLAP tear. The SLAP lesion can also be an acute injury that can be caused by a traction type of injury or a compressionshear type of injury from the humeral head. In general, the examination tests described to identify superior labral lesions attempt to pull on the torn structures with tension and rotation or push on the torn structures with the humeral head. Patients with SLAP tears often complain of a deep pain in the shoulder. The tests are positive if this deep pain is produced during the provocative maneuver. As with all tests, diagnostic injections are critical to confirm the presumed diagnosis. Figure 4-20. Speed’s test for long head of biceps pathology.
The active compression test described by O’Brien is one of the more commonly performed tests. It is accomplished by standing behind the patient. The patient is asked to forwardflex the arm to 90 degrees, with the elbow in full extension against resistance (Speed’s test). The arm is then adducted 10 to 15 degrees medially to the sagittal plane of the body, with the arm internally rotated (thumb down), and resistance is again applied. With the arm in the same position, the test is repeated with the palm facing upward. The test is considered positive if pain is elicited during the maneuver with the thumb pointing down and relieved with the palm facing up (Fig. 4-22).35 This test will often be positive with impingement and with acromioclavicular pathology, so it is important to ask the patient to localize the pain during the test. The results have been shown to be positive in 95% of patients with superior labral pathology. Often, we have also found the test positive with other labral pathology. The O’Driscoll SLAP test is performed with the patient supine or upright. The shoulder is maximally abducted and externally rotated. From this position, a moving valgus stress is applied in an attempt to push the humerus against the superior labrum.20 Pain is considered a positive response. This is similar to the compression-rotation test as described by Snyder and coworkers,34 except that the arm is placed in maximum abduction and external rotation. We have found this test to be sensitive but not specific. The crank test, as described earlier, may also be found positive in SLAP tears.
Figure 4-21. Yergason’s test for biceps pathology.
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There are many alternative SLAP tests and most produce fairly good sensitivities and specificities, but it must be stressed that none of the tests is absolutely diagnostic of a
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A
B
Figure 4-22. O’Brien’s active compression test for superior labral anterior-posterior (SLAP) lesions. A, Test performed with palm down. B, Test repeated with palm up.
SLAP tear. Any of the positive tests can be repeated after the injection of 10 mL of 1% lidocaine into the glenohumeral joint. Abatement of pain after the injection is further confirmation of intra-articular involvement. The results of these tests, with an accurate history and comprehensive examination, can be helpful in arriving at an accurate diagnosis.
GLENOHUMERAL STABILITY ASSESSMENT Glenohumeral instability is assessed by provocative maneuvers, such as an apprehension sign. It is also assessed by translation, anteriorly and posteriorly, of the humeral head in the glenoid fossa, as well as inferior translation with a sulcus sign. During these maneuvers, it is important to ask the patient whether there is any reproduction of the symptom complex. It is not uncommon for the throwing athlete to present with shoulder pain and have an underlying degree of subtle anterior instability. Similarly, it is not uncommon for the hyperlax and hypermobile patient to have an element of multidirectional instability. Many patients also present with arm weakness or heaviness, the so-called dead arm syndrome.36-38 Therefore, it is imperative to consider the patient’s pain symptoms during the examination as an important aspect of any provocative testing. Initially, the patient should be as relaxed as possible. It is often prudent to begin the stability assessment with the
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contralateral or uninvolved shoulder to gain the patient’s confidence during the examination. The stability assessment begins with the load and shift examination. When assessing the amount of translation, it is important to ensure that the humeral head is initially reduced concentrically into the glenoid fossa (i.e., loaded). In patients with significant laxity, the humeral head may have a resting position that is nonconcentric. Hence, at the commencement of any stress testing, the humeral head must be grasped and pushed into the glenoid fossa to ensure its reduction in neutral position.39 Once the humeral head is loaded, directional stresses may be applied. To perform this maneuver, the examination initially involves assessment of the patient sitting and the examiner located beside and behind the side to be examined. The examiner places his or her hand over the shoulder and scapula to steady the limb girdle and then, with the opposite hand, grasps the humeral head. As the head is loaded, anterior and posterior stresses are applied and the amount of translation is noted (Fig. 4-23). Next, the elbow is grasped and inferior traction is applied. The area adjacent to the acromion is observed and dimpling of the skin may indicate a sulcus sign (Fig. 4-24). A positive sulcus sign may be seen in patients with multidirectional instability (MDI), but also can be positive in patients with combined labral and rotator interval lesions. It is important to differentiate between generalized laxity and instability. A positive test should reproduce the patient’s symptoms. An increased sulcus sign as compared with the asymptomatic shoulder is helpful and should be documented by recording how much the humeral head is translated inferiorly from the acromion (in millimeters). If a positive sulcus sign is identified, the test should then be repeated with the arm externally
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A Figure 4-24. Sulcus sign.
B Figure 4-23. Determining the amount of translation. A, Sitting anterior load shifting. B, Sitting posterior load shifting.
A
rotated 20 to 30 degrees; if still positive, it can be suggestive of a rotator interval deficiency. Glenohumeral translation is also assessed with the patient supine. The arm is grasped in the position of approximately 20 degrees of abduction and forward flexion in neutral rotation. The humeral head is loaded and posterior and anterior stresses are applied. Inferior stress is applied again, noting the sulcus sign (Fig. 4-25). The accuracy of this test will depend not only on the examiner’s skill but on the ability of the patient to relax. In some patients with associated tendinitis, it is too painful to grasp the humeral head between the thumb and fingers. In this situation,
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B Figure 4-25. Load shift test. A, Supine anterior load shift test B, Posterior load shift test.
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grasping the upper arm distally to the shoulder may be the only method of assessing translation but is less reliable. It is helpful to have a grading system of translations so that the translation can be understood in relation to any instability pattern that may or may not be present. It is impractical to use distances or percentages. Two important situations may occur during this examination. First, the examiner may feel the humeral head ride up to the face of the glenoid but not over the rim (grade I). Second, the head may be felt riding over the rim but reduces when the stress is released (grade II). In some cases, at least under anesthesia, once the stress is released, the head sometimes remains dislocated. For purposes of simplicity, this should probably not receive a separate grade. It is important during these maneuvers to ask the patient if this in any way reproduces the symptom complex. If affirmative, this might be a significant clue toward diagnosis and direction of instability, especially for posterior instability. Anterior and posterior drawer tests have also been described.40 These are variations of the glenohumeral translation test analogous to the Lachman test of the knee. They are performed with the patient in the supine position to make measurements more reliable. The affected shoulder is held in 80 to 120 degrees of abduction, 0 to 20 degrees of forward flexion, and 0 to 30 degrees of lateral rotation. While pressing the scapular spine forward with counterpressure on the coracoid process, the relative movement between the fixed scapula and the moveable humerus can be appreciated. Occasionally, a positive grind test can be felt during this maneuver, noting labral pathology. The posterior drawer test is performed with the elbow at 120 degrees of flexion and the shoulder in 80 to 120 degrees of abduction and 20 to 30 degrees of forward flexion. Again, the scapula is stabilized, and a posterior directed force is placed on the humeral head with the thumb.
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of the arm when subluxation or dislocation occurs is abduction in external rotation. The apprehension test for anterior instability can be performed with the patient in the supine or seated position, although maximum muscle relaxation is best achieved with the patient supine. With the patient sitting, the examiner stands behind the shoulder to be examined. To assess the patient’s left shoulder, the examiner raises the patient’s arm to 90 degrees of abduction and begins to rotate the humerus externally. The right hand of the examiner is placed over the humeral head, with the thumb pushing from posterior for extra leverage and with the fingers anterior to control for any sudden instability episode that may occur (Fig. 4-26). With increasing external rotation and controlled general forward pressure exerted against the humeral head, an impending feeling of anterior instability may be produced— an apprehension sign. An apprehensive look may appear on the patient’s face as he or she contracts his or her muscles to prevent dislocation or, if the stress is continued, he or she may volunteer that the shoulder feels like it will come out. Pain alone is not a positive apprehension sign, although it is often present. The apprehension test can be repeated with the patient supine (Fig. 4-27). The shoulder to be examined is positioned so that the scapula is supported by the edge of the examining table and the proximal humerus is then stressed in varying degrees of abduction and external rotation, again attempting to reproduce impending instability. In the supine position, the body acts as a counterweight. The
Significant expansion of information about the athlete’s shoulder has come from advances in arthroscopy.41 During arthroscopy, particularly under general anesthesia, an appreciation of glenohumeral translation can be obtained. This is sometimes important when completing the examination of the athlete who has a confusing diagnosis and has arrived at the stage of surgical reconstruction.42 The next phase of stability assessment is to attempt reproduction of the symptom complex by eliciting apprehension with certain provocative positions of impending subluxation or dislocation. This is especially applicable for anterior instability. The apprehension test is an evaluation of the patient’s sense of pending anterior subluxation or dislocation with the arm in stressed external rotation abduction.38,43 The role of pain needs to be interpreted, because frequently a patient may not be apprehensive in this position but may only experience pain. The usual position
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Figure 4-26. Apprehension sign for anterior instability in the sitting position.
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not with apprehension. A positive relocation test for pain located in the posterior aspect of the shoulder is suggestive of internal impingement between the posterosuperior labrum and infraspinatus tendon. This is an important differentiation because the problem is likely the result of posterior capsular tightness and not anterior instability. The positive relocation test allows greater external rotation in the abducted position, with less pain.
Figure 4-27. Apprehension sign for anterior instability in the supine position.
edge of the table serves as the fulcrum and the arm as the lever. When the apprehensive position is located, note is taken of the amount of external rotation. With the arm in this position, a posterior stress may be exerted on the proximal humerus and the apprehension may disappear, allowing external rotation before emergence of the apprehension sign. The relocation test can be done and has two possible results—at the apprehension point, the humeral head is subluxated slightly and pushing it posteriorly causes reduction, or the posteriorly directed pressures act as a supportive buttress anteriorly to give the patient more confidence, preventing apprehension (Fig. 4-28). The relocation test was originally described in the presence of pain only and
Figure 4-28. Relocation test for internal impingement. The relocation maneuver eliminates pain in the posterior shoulder and permits increased external rotation. For anterior instability, the relocation maneuver eliminates apprehension.
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If the arm is suddenly released when stressed with external rotation and abduction, the patient has a substantial increase in pain, which may be referred to as a release test. This may be caused by the humeral head jumping forward on release of the posteriorly applied stress. The pain can also be augmented with external rotation and abduction by pulling forward on the back of the arm (augmentation test). These findings may be present but are not necessarily related to nor represent the classic apprehension sign. Their value, however, is in the differentiation of impingement or anterior subluxation as the source of pain. Posterior instability may present with subluxation rather than dislocation. Pain may also be a contributing factor. Most patients can demonstrate the position that reproduces their symptoms. Having ascertained the compromising maneuver, the examiner may attempt to reproduce the instability by manually duplicating the stresses. Because this is usually a painless subluxation that easily reduces, posterior apprehension is not commonly present and, therefore, is not a reliable sign. With posterior stresses, patients who are painful may resist, which is sometimes erroneously interpreted as apprehension. The Jahnke or jerk test, when positive, is excellent for diagnosing posterior instability patterns. The examiner adducts and internally rotates the shoulder and then applies a posterior stress. If unstable, the humeral head will subluxate posteriorly. Next, the shoulder is brought back from horizontal adduction while maintaining a posterior force on the humerus from the elbow. As the shoulder returns to neutral, a clunk or visible reduction may be felt and heard as the shoulder reduces (Fig. 4-29).20 In posterior instability, the patient who cannot demonstrate the instability may present a diagnostic challenge. It is not uncommon for the patient only to demonstrate pain on posterior stress testing of the shoulder, without any obvious translational abnormalities. This subset of patients may have only a labral tear, without significant capsular redundancy. At times, a click may be felt on posterior stress testing suggesting a posterior labral tear. Therefore, pain reproducing the patient’s symptoms may provide the only diagnostic clue. Patients with inferior instability may state that the distal traction on the arm reproduces their symptom complex, suggesting underlying multidirectional instability.44,45 Comparison with the contralateral extremity is always performed following the examination.
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and wrist are noted. Evaluation of muscle mass and tone, and strength, is performed during the palpation part of the examination. The addition of evaluation of wrist extension, finger abduction and adduction, thumb abduction, and elbow extension can provide a quick assessment of the health of the cervical roots. Cervical spine radiculopathy can mimic that of intrinsic shoulder disease (e.g., C5 radiculopathy can mimic a rotator cuff tear).46-48 Spurling’s test is helpful to determine cervical disease (Fig. 4-30). The neck is flexed and rotated to one side, with corresponding compression to elicit pain.49 In the absence of tenderness of the posterior cervical spinous processes to palpation, and in the presence of a negative Spurling’s test, cervical spine pathology and radiculopathy can usually be excluded.
VASCULAR EXAMINATION A
The vascular examination consists of palpation of the pulses at the wrist and elbow, along with an assessment of vascular changes from dystrophy, such as swelling, discoloration, and lack of sweating. There are also tests to determine thoracic outlet syndrome. Adson’s maneuver is performed with the shoulders extended, breath held, neck extended, and chin turned to the same side. The arm is in a slightly abducted and extended position. Diminution of a palpable pulse at the wrist is considered positive for thoracic outlet syndrome (Fig. 4-31). Other thoracic outlet tests are less
B Figure 4-29. Jerk (Jahnke) test for posterior instability. A, Shoulder is adducted with posterior force on the shoulder. B, Clunk or visible reduction as shoulder is brought back to neutral.
NEUROLOGIC EXAMINATION Any athlete who presents with shoulder pain and/or weakness should have a thorough neurologic examination. It is however, common for many athletes who throw, swim, and serve to present with dysesthesias in their extremities. For example, this is a common presentation with instability patterns. The timing of performing a neurologic examination may vary. It is frequently helpful to carry out the examination during range-of-motion assessment because strength testing is done almost concurrently, and it seems appropriate to complete the sensory and reflex examinations at that time. Normally, a dermatomal sensory examination is performed in the usual manner. Deep tendon reflexes at the elbow
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Figure 4-30. Spurling’s test.
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A
Figure 4-31. Adson’s maneuver for thoracic outlet syndrome.
reliable; perhaps the most helpful is provocative testing. The Roos test is performed with the patient standing or sitting, with both shoulders in abduction and external rotation. With the arms above the head, the patient is asked to open and close each fist repetitively to reproduce the symptoms distal to the forearm (Fig. 4-32).50 This often causes an aching fatigue, suggestive of thoracic outlet syndrome.
SUMMARY Athletes with shoulder injuries often present a diagnostic dilemma. If the examiner systematically approaches the history to classify the patient as having specific symptom patterns and performs a thorough physical examination, paying particular attention to how the assessment relates to the patient’s symptomatology, an accurate diagnosis can usually be made. Specifically, the initial event or injury is a critical aspect of the history and a thorough understanding is helpful before beginning the examination. Management techniques are obviously predicated on an accurate diagnosis. Often, patients can relate the exact mechanism of injury and actually have a clear understanding of their symptom pattern. However, with increasing demands from an athletic population, many patients present with unclear histories of their symptoms. The importance of using injections and comparing with the asymptomatic shoulder to confirm examination findings cannot be overstated. If care is taken during the examination to be thorough and organized, the correct diagnosis can be reached.
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B Figure 4-32. Roos test for thoracic outlet syndrome.
References 1. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220, 1988. 2. Jobe FW, Bradley JP: Rotator cuff injuries in baseball: Prevention and rehabilitation. Sports Med 6:377, 1988. 3. Butters KP, Rockwood CA Jr: Office evaluation and management of the shoulder impingement syndrome. Orthop Clin North Am 19:755, 1988. 4. Nirschl RP: Shoulder tendinitis. In Pettrone FA (ed): Symposium on Upper Extremity Injuries in Athletes (American Academy of Orthopaedic Surgeons). St. Louis, Mosby, 1986.
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5. Hawkins RJ, Hobeika P: Impingement syndrome in the athletic shoulder. Clin Sports Med 2:391, 1983. 6. Neer CS II: Impingement lesions. Clin Orthop 173:70, 1983. 7. Neer CS II: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg Am 54:41, 1972. 8. Neer CS II, Welsh RP: The shoulder in sports. Orthop Clin North Am 8:583, 1977. 9. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics and tennis. Clin Sports Med 2:247, 1983. 10. Hawkins RJ, Bell RH: Collagen analysis in patients with multidirectional instability. Presented at the AOSSM Specialty Day Meeting, Anaheim, CA, March 1991. 11. Hawkins RJ, Hobeika P: Physical examination of the shoulder. Orthopedics 10:1270, 1983. 12. Drez D Jr: Suprascapular neuropathy in the differential diagnosis of rotator cuff injuries. Am J Sports Med 4:43, 1976. 13. Burkart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404, 2003. 14. Codman EA: Normal motions of the shoulder joint. In Codman EA (ed): The Shoulder. Boston, Thomas Todd, 1934, p 32. 15. Freeman L, Monroe RR: Abduction of the arm in the scapular plane: Scapular and glenohumeral movement. J Bone Joint Surg Am 48:1503, 1966. 16. Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 58:195, 1976. 17. Jobe FW, Jobe CM: Painful athletic injuries of the shoulder. Clin Orthop 173:117, 1983. 18. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192, 1986. 19. Lombardo SJ, Jobe FW, Kerlan RK, et al: Posterior shoulder lesions in throwing athletes. Am J Sports Med 5:106, 1977. 20. Krishnan SG, Hawkins RJ, Warren R: The Shoulder in the Overhead Athlete. Philadelphia, Lippincott Williams & Wilkins, 2004. 21. Hoyt WA Jr: Etiology of shoulder injuries in athletes. J Bone Joint Surg Am 49:755, 1967. 22. Rockwood CA, Green DP: Fractures in Adults. Philadelphia, JB Lippincott, 1984. 23. Shields CL, Glousman RE: Open management of rotator cuff tears. In Grana WA (ed): Advances in Sports Medicine and Fitness, vol 2. Chicago, Year Book, 1989, p 223. 24. Walton J, Mahajan S, Paxinos A, et al: Diagnostic value of tests for acromioclavicular joint pain. J Bone Joint Surg Am 86:807, 2004. 25. Hurley JA, Anderson TE: Shoulder arthroscopy: Its role in evaluating shoulder disorders in the athlete. Am J Sports Med 18:480, 1990. 26. Colachis SC Jr, Strohm BR: Effect of suprascapular and axillary nerve blocks and muscle force in upper extremity. Arch Phys Med Rehabil 52:22, 1971. 27. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 28. Scheib JS: Diagnosis and rehabilitation of the shoulder impingement syndrome in the overhead and throwing athlete. Rheum Dis Clin North Am 16:971, 1990.
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29. Yergason RM: Supraspinatus sign. J Bone Joint Surg 13:60, 1931. 30. Tennent TD, Baech WR, Meyers JF: A review of the special tests associated with shoulder examination, Part I: The rotator cuff tests. Am J Sports Med 31:154, 2003. 31. Tennent TD, Baech WR, Meyers JF: A review of the special tests associated with shoulder examination, Part II: laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med 31:301, 2003. 32. Crenshaw AII, Kilgore WE: Surgical treatment of bicipital tenosynovitis. J Bone Joint Surg Am 48:1496, 1966. 33. Bennett WF: Specificity of the Speed’s test: Arthroscopic technique for evaluating the biceps tendon at the level of the bicipital groove. Arthroscopy 14:789, 1998. 34. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274, 1990. 35. O’Brien SJ, Pagnani MJ, Fealy S, et al: The active compression test: A new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med 26:610, 1998. 36. Hastings DE, Coughlin LP: Recurrent subluxation of the glenohumeral joint. Am J Sports Med 9:352, 1981. 37. Protzman RR: Anterior instability of the shoulder. J Bone Joint Surg Am 62:909, 1980. 38. Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863, 1981. 39. Hawkins RJ, Schutte JP, Huckell GH, Abrams J: The assessment of glenohumeral translation using manual and fluoroscopic techniques. Orthop Trans 12:727, 1988. 40. Gerber C, Ganz R: Clinical assessment of instability of the shoulder with special reference to anterior and posterior drawer tests. J Bone Joint Surg Br 66:551, 1984. 41. Pappas AM, Goss TP, Kleinman PK: Symptomatic shoulder instability due to lesions of the glenoid labrum. Am J Sports Med 11:279, 1983. 42. Cofield RH, Irving JF: Evaluation and classification of shoulder instability with special reference to examination under anesthesia. Clin Orthop 223:32, 1987. 43. Zarins B, Rowe CR: Current concepts in the diagnosis and treatment of shoulder instability in athletes. Med Sci Sports Exerc 16:444, 1984. 44. Neer CS II: Involuntary inferior and multidirectional instability of the shoulder: Etiology, recognition and treatment. Instr Course Lect 34:232, 1985. 45. Neer CS II, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897, 1980. 46. Bateman JE: Neurologic painful conditions affecting the shoulder. Clin Orthop 173:44, 1983. 47. Bennett RM: The painful shoulder. A four-article symposium. Postgrad Med 73:153, 1983. 48. Bowling RW, Rockar PA Jr, Erhard R: Examination of the shoulder complex. Phys Ther 66:1866, 1986. 49. Spurling RG, Scoville WB: Lateral rupture of the cervical intervertebral discs. Surg Gynecol Obstet 78:350, 1944. 50. Roos DB: Congenital anomalies associated with thoracic outlet syndrome. Anatomy, symptoms, diagnosis, and treatment. Am J Surg 132:771, 1976.
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CHAPTER 5 Diagnostic Imaging of the
Shoulder Complex Martin L. Schwartz and D. Dean Thornton
Evaluation of shoulder disorders has become much easier because of advances in imaging techniques. Continued refinement of magnetic resonance imaging (MRI) and computed tomography (CT) hardware and software have significantly improved the sensitivity and specificity of diagnosing pathologic conditions of the shoulder. Increasingly accurate imaging diagnosis of shoulder disorders has decreased the number of unnecessary arthroscopic procedures while providing important information that guides appropriate surgical intervention. This chapter will present the state of the art shoulder imaging available to the orthopedic surgeon, sports medicine physician, and radiologist.
Included in this study are internal and external rotation views, an axillary view, and weight-bearing views. CT is an excellent imaging technique for evaluation of bony abnormalities such as fractures; however, like conventional radiographs, it provides limited information regarding soft tissues. With the widespread availability of multislice helical CT scanners, sophisticated reconstructed images can be obtained in two and three dimensions (2D and 3D). A slice thickness as small as 1 mm can be used and yields highquality reconstructed images. Generally, the examination is performed with the shoulder in external rotation and the patient supine. Two-dimensional reconstructed images are usually performed in the oblique sagittal and coronal planes. Three-dimensional reconstructions allow for image rotation into any plane. Postprocessed images can be viewed on workstations with multiple window levels.
IMAGING TECHNIQUES After a thorough clinical examination of the shoulder, conventional radiographs should be obtained, with a minimum of three views—anteroposterior internal and external rotation, as well as axillary views. Additional views may be obtained depending on the specific pathology involved. At our institution, the thrower’s series consists of five radiographs; these include the West Point, axillary, Stryker notch, and internal and external rotation views. Occasionally, an acromial profile view is added. These radiographs should enable the clinician to evaluate the skeletal structures and to exclude most common fractures and dislocations. It must be stressed that conventional radiographs of the shoulder are of limited benefit in the evaluation of soft tissues, with the exception of calcification in the rotator cuff. If conventional radiographs are negative, the next diagnostic imaging test required will vary according to the specific condition that the clinician needs to confirm based on the mechanism of injury and physical examination.
MRI is the most powerful imaging tool available to the clinician when there are questions regarding the status of the osseous and soft tissue components of the shoulder. MRI can provide an overview of pathology when there is uncertainty in the clinical examination results. MRI can also be directed to answer specific clinical questions. There are many options to consider when referring a patient for MRI. There are differing levels of magnet strength and quality; most current MR scanners offer 1.5-tesla (T) imaging. Older MR units may be 1.0 T, but more powerful 3.0-T scanners are becoming increasingly common in larger centers. Claustrophobic or large patients may require the use of an open MR unit, which can range in strength from 0.2 to 0.7 T. Newer, even higher strength (up to 1.5 T), open MR units are becoming available. There is a correlation between magnet strength and image quality, but even lowfield strength magnets can produce good images if used properly. In general, a high-field MRI unit should be used whenever possible.1 MRI allows for direct imaging of the important soft tissue structures of the shoulder, such as the rotator cuff, labrum, and glenohumeral ligaments, while providing information about osseous structures that is complementary to that obtained by radiography and CT. The cross-sectional nature of MRI allows for the examination of anatomic structures in multiple planes.
Conventional arthrography is seldom used in isolation because of the advances in MR arthrography. It can be useful for patients who have a contraindication to MRI, such as those with a cardiac pacemaker or other device that is not MRI compatible. The procedure is performed using sterile technique and fluoroscopic guidance, with the patient in the supine position and the shoulder in external rotation. Following administration of a local anesthetic, a 22-gauge spinal needle is placed into the joint. For single-contrast arthrography, approximately 15 mL of iodinated contrast is injected into the joint. For double-contrast arthrography, injection of 6 mL of contrast is followed by injection of 12 mL of air. Five radiographs are obtained after controlled exercise.
MR arthrography is another important tool that can be used in the diagnostic evaluation of the shoulder. The addition of intra-articular contrast provides another layer of detail to the MR examination. Shoulder arthrography is 73
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performed in the customary way, using a dilute solution of gadolinium. Injection of contrast accomplishes several purposes. It ensures the presence of joint fluid, which outlines intra-articular structures such as the labrum and makes them more conspicuous. The joint is distended, which forces fluid into the tears and leaks that are being sought (e.g., rotator cuff tears, labral tears, capsular disruptions). The unique MR properties of gadolinium allow for the detection of small amounts of contrast on MRI, with differentiation from other fluid around the joint that may be present. Performed properly, MR arthrography is a quick and easy way to obtain additional information from the shoulder MRI examination.
imaging is required. Complex humeral fractures can be further evaluated using CT3,4 and, to a lesser degree, MRI. Newer, multislice, helical CT scanners can provide not only high-quality axial images but can also produce 2D and 3D reconstructed views in any plane. The reconstructed images allow the surgeon to visualize and manipulate these fractures using sophisticated software and high-quality monitors. MRI is particularly useful for occult fractures in which radiographs are negative. A typical low-signal pattern is seen on T1-weighted images, with increased T2 signal on short tau inversion recovery (STIR) or T2-weighted fat-suppressed images. The fracture lines can range from simple and linear to complex and stellate.
In those patients who cannot undergo MRI of the shoulder for some reason (e.g., cardiac pacemaker, large body habitus), CT arthrography can provide much of the same diagnostic information. Conventional arthrography is first performed using a single-contrast or air contrast technique. As with MR arthrography, the intra-articular contrast outlines the important anatomic structures and exposes tears and leaks to greater advantage. Transverse CT scans are then acquired through the region of interest. Multiplanar reconstruction images can be produced, which can approximate the appearance of the images obtained by MRI.
Dislocations, particularly posterior in position, can be problematic with conventional radiograph analysis. Subtle dislocations or subluxations can be missed if only anteroposterior internal and external rotation views are obtained. For this reason, an axillary view should be obtained when dislocation is suspected (Fig. 5-1). In the acute setting, CT can be helpful in identifying subtle dislocations as well any associated fractures of the humeral head or glenoid (see Fig. 5-1). CT and MRI can both be useful in the evaluation of the osseous and soft tissue changes associated with chronic dislocation.
Sonography or ultrasound (US) of the shoulder can provide some useful information to the clinician. Partial or fullthickness rotator cuff tears can be identified accurately with US. Advantages of US include its relatively low cost compared with MRI and lack of ionizing radiation used for radiography and fluoroscopy. There are, however, several important limitations of US in the examination of the athlete’s shoulder. Evaluation of structures other than the rotator cuff is limited. Specifically, the labroligamentous structures are not well demonstrated. The sonographic examination of the shoulder can be difficult and is highly operator dependent. In general, clinicians are not as comfortable viewing shoulder US images as they are with radiography or MRI.
IMAGING OF SPECIFIC PATHOLOGIC CONDITIONS Fracture and Dislocation In 1970, Neer2 published his classic paper on acute proximal humeral fractures, showing that the prognosis depended not only on the number of fracture fragments but also on the amount of displacement and angulation. Minimally displaced fractures could be treated without surgery; however, significant separation of fragments or rotation required surgery to prevent chronic changes and loss of function. If a fracture or dislocation is suspected after physical examination, conventional radiographs should be obtained. Most fractures will be obvious on this examination, and no further
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MR arthrography is the diagnostic imaging test of choice for patients with chronic dislocation to evaluate the glenoid labrum and capsular structures. Often, chronic injuries to the labrum and bony glenoid are seen. MR arthrography can also be used in cases of acute dislocation in which specific labral and capsular changes occur. These findings will be discussed later in the chapter.
Bone and Articular Cartilage Abnormalities Osteoarthritis is a common condition seen in the shoulder. Loss of articular cartilage leads to osteophyte formation, subchondral cysts, and synovitis. Radiographs (and CT) will show joint space narrowing, sclerosis of the subchondral bone, subchondral cysts, and osteophyte formation. MRI demonstrates a subchondral low signal on T1-weighted images, with increased T2 signal caused by cystic changes. Other conditions that mimic these findings include inflammatory arthritis, synovitis, septic arthritis, and neuropathic arthritis. The findings can be seen in conjunction with other shoulder pathology, such as rotator cuff tears. Avascular necrosis (AVN) or osteonecrosis most often occurs in the superomedial portion of the humeral head. On MRI, the finding of low-signal serpiginous lines in the subchondral bone in this location is virtually diagnostic (Fig. 5-2). With advanced cases, there may be flattening of the humeral head, which may progress to collapse similar to that seen in the hip. Osteochondral lesions are seen in conjunction with shoulder trauma.5 Both the articular cartilage and underlying
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B
Figure 5-1. Posterior shoulder dislocation. A, Anteroposterior radiograph. There is a subtle indentation on the humeral head (arrow), but the findings are equivocal. B, Axillary view. The posterior dislocation of the humeral head is clearly seen. The anterior humeral head is impacted against the posterior rim of the glenoid (arrow). C, Axial computed tomography (CT) scan in a different patient. A fracture of the lesser tuberosity (arrow) may accompany posterior dislocation.
bone may be injured. This finding is most commonly demonstrated in the anterior glenoid, but can occur posteriorly or on the humeral head. The abnormality can range in size from just a few millimeters to a large area of several centimeters of cartilage loss. The best imaging modality for these abnormalities is to use a cartilage-sensitive MRI sequence (gradient or fat-suppressed proton density) in the axial and coronal planes, intra-articular contrast, or both (Fig. 5-3). The reactive changes in the underlying subchondral bone can best be seen on T2 fat-suppressed images.
fat-suppressed images.6 The loose bodies can range in size from a few millimeters to more than 1 cm. They can occur anywhere in the joint space but are most commonly observed anteriorly and inferiorly (Fig. 5-4). Care must be taken not to mistake air bubbles inadvertently introduced at the time of joint injection for loose bodies. These are usually located in a nondependent position anterior in the joint with the patient supine on the MRI table.
Loose bodies can be seen when an injury to the cartilage or bone has occurred. Both cartilaginous and bony loose bodies are best detected using MR arthrography with T1
The diagnosis of adhesive capsulitis is usually based on the clinical examination. Often, patients presenting with this condition have undergone previous surgery, have had
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A
B
Figure 5-2. Avascular necrosis of the humeral head. A, Coronal proton density MR image. A serpiginous low-signal line is present in the subchondral bone of the humeral head (arrow). B, Coronal short tau inversion recovery (STIR) image. Bone marrow edema is found around the low-signal abnormality. Note also the mild flattening of the humeral head (arrow).
Figure 5-3. Osteochondral lesion of the glenoid; coronal T2-weighted fat-suppressed magnetic resonance arthrogram. Focal chondral defect in the anterior inferior glenoid is associated with subchondral edema (arrow).
Figure 5-4. Loose bodies; axial T1 magnetic resonance arthrogram. Multiple small osteochondral bodies (arrow) are present in the subscapular recess of the joint space.
multiple joint injections, or are chronic dislocators. Imaging confirmation is obtained when the patient undergoes joint injection for MR arthrography. The total volume of the joint space is reduced, limiting the quantity of contrast that can be injected. The patient will also complain of pain
during the injection, especially when the volume end point is reached. MRI shows an irregular, small, axillary recess that is markedly reduced in volume.7,8 If the patient has a contraindication to MRI, a conventional arthrogram can be obtained to confirm the diagnosis.
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Bennett Lesion When an individual presents with posterior shoulder pain, particularly with overhead motion, a Bennett lesion should be considered. This condition, also referred to as thrower’s exostosis, results from posterior capsular traction on the glenoid. Calcification is found adjacent to the posterior glenoid, but this finding can be subtle and is often hard to visualize on conventional radiographs. MRI shows an area of very low signal adjacent to the posterior glenoid.9 CT can be diagnostic, with the calcification nicely demonstrated as conforming to the contour of the glenoid or in the adjacent capsular soft tissues (Fig. 5-5).10,11
Labral Injury Most glenoid labrum abnormalities are caused by shoulder trauma, particularly dislocation. The humeral head moves anteriorly or posteriorly relative to the glenoid, affecting the labrum and stretching capsular structures. MR arthrography has become the imaging procedure of choice for diagnosis of these conditions. Most complex labral injuries involve the anterior labrum and will be discussed later. A Bankart lesion is defined as an anterior labral disruption with tearing of the attached periosteum, usually as a result of anterior dislocation. On MR arthrography, contrast flows into the defect created by the absence of the anterior labrum.12 There is often a Hill-Sachs fracture of the posterolateral aspect of the humeral head. If the bony glenoid is involved the abnormality is then referred to as a bony Bankart lesion. The abduction external rotation (ABER)
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sequence can often demonstrate this abnormality as the labrum and periosteum are pulled away from the glenoid by the traction placed on these structures in this position (Fig. 5-6).13 There are several Bankart variants that involve the anterior labrum; these are based on the type of detachment of the anterior labrum and capsule from the glenoid. A Perthes lesion involves detachment of the anterior labrum from the glenoid, with preservation of an intact attachment to the periosteum (unlike in the Bankart lesion).14 The anterior labrum, although detached, may remain in place, making the tear difficult to see on routine MR sequences. Again, the ABER view is often the most helpful in diagnosing this problem because it accentuates the separation between labrum and glenoid (Fig. 5-7). The anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion involves an anterior labral detachment with rotation of the labrum 90 degrees medially and an avulsion of the inferior glenohumeral labroligamentous complex, with an intact periosteum still attached to the labrum.15 If chronic, the labrum may scar down in this medially displaced location (Fig. 5-8). Axial MR arthrographic and ABER sequences are most helpful to visualize these findings. The Bankart lesion and its variants involve some degree of anterior instability. The glenolabral articular disruption (GLAD) lesion consists of an articular cartilage defect in the anterior glenoid, with a partial tear of the anterior labrum (Fig. 5-9).15 Axial and coronal MR arthrographic images often show both
B
Figure 5-5. Bennett lesion. A, Axial T1 magnetic resonance arthrogram. A focus of low signal (arrow) is found at the posterior capsular insertion on the glenoid. B, Axial computed tomography (CT) scan. This confirms the calcific nature of the low signal (arrow).
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A
A
B
B
Figure 5-6. Bankart lesion. A, Axial T1 magnetic resonance arthrogram. The anterior labrum is torn and detached from the anterior glenoid (arrow). B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. The ABER position puts traction on the anterior labroligamentous structures. Note the increased separation of the anterior labrum (arrow) from the glenoid.
Figure 5-7. Perthes lesion. A, Axial T1 magnetic resonance arthrogram. No definite abnormality is seen in this patient suspected of having a labral tear. B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. The ABER position reveals the anterior labral tear, although the labrum remains attached to the scapular periosteum (arrow).
abnormalities, especially if cartilage protocols are used. This lesion is considered stable.
whether the bony glenoid is involved. There may be a reverse Hill-Sachs lesion of the anteromedial humeral head in these patients. The posterior band of the inferior glenohumeral ligament and the posterior capsule may also be affected. Axial and ABER images show detachment of the labrum from the glenoid, with contrast filling the space (Fig. 5-10). Posterior labral tears also occur in association with glenoid dysplasia.16
Posterior labral tears are generally caused by posterior dislocations of the humeral head. The most common mechanism of injury is the result of a direct anterior blow to the humeral head or a seizure. These are often called reverse Bankart or bony Bankart lesions, depending on
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A Figure 5-8. Anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion; axial T1 magnetic resonance arthrogram. In this patient, with a history of recurrent anterior shoulder dislocation, the anterior labrum is deformed and displaced medially (white arrow) along the anterior margin of the glenoid. Note the Hill-Sachs deformity of the posterior humeral head (black arrow), confirming the history of dislocation.
B Figure 5-10. Posterior labral tear. A, Axial T1 magnetic resonance arthrogram. There is a tear of the posterior labrum (arrow), with contrast extending through the tear into a small paralabral cyst. B, Axial gradient sequence. In a different patient, a posterior labral tear is associated with a large paralabral cyst that extends to the spinoglenoid notch (arrow).
Figure 5-9. Glenolabral articular disruption (GLAD) lesion; axial T1 magnetic resonance arthrogram. A small, focal, chondral defect of the anterior glenoid (arrow) is associated with a partial nondisplaced tear of the anterior labrum.
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Superior labral anterior-posterior (SLAP) lesions can be simple or complex.17 There are nine different classifications of SLAP lesions, depending on the adjacent structures involved. Types I to IV involve tears of the superior labrum with or without involvement of the biceps tendon or biceps anchor. Types V to IX show extension into different adjacent soft tissues. On coronal MR images, contrast is seen entering the tear of the superior labrum, with associated increased signal
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in adjacent structures on T2-weighted images (Fig. 5-11). Care must be taken not to mistake the normal sublabral foramen that can exist between the superior labrum and glenoid for a SLAP lesion. Approximately 3% to 5% of all labral tears are associated with a paralabral cyst. Occasionally, the labral tear will heal but the cyst will persist. The cysts can vary in size, ranging from a few millimeters to several centimeters in the dissecting type.18 If there is a connection between the labral
tear and the cyst, some contrast may be seen in the cyst as high signal on T1-weighted fat-suppressed images. The cyst will be low signal on T1-weighted fat-suppressed images if there is no connection. Both will show high signal on T2-weighted images. A paralabral cyst associated with a superior labral tear may extend to the suprascapular notch. If the cyst compresses the suprascapular nerve, pain and weakness can develop in the supraspinatus and infraspinatus muscles. If the cyst relates to a posterior labral tear, it may extend to the spinoglenoid notch, where it may affect the nerve supply to the infraspinatus only (Fig. 5-10).
Glenohumeral Ligament Injury The inferior glenohumeral ligament (IGHL) is the most commonly torn ligament in the shoulder joint. IGHL tears usually occur with anterior dislocations because they also affect the inferior joint space. The IGHL forms the axillary pouch or recess and, when torn, the fibers are discontinuous on coronal MR arthrographic images. There may be extravasation of contrast into the adjacent soft tissues. Occasionally, the ligament is just sprained and not completely torn, resulting in stretching or thickening of the IGHL without disruption. These findings can also be seen on noncontrast MR images, particularly when using the ABER view.19
A
The humeral avulsion of the glenohumeral ligament (HAGHL) lesion occurs when the IGHL is torn from the humerus or when there is an avulsion fracture at the humeral attachment. This lesion occurs with anterior-inferior dislocation of the humeral head. The IGHL fibers are discontinuous at the humeral interface and the normally U-shaped axillary recess becomes J-shaped (Fig. 5-12).20 If there is bony avulsion, there will be edema in the donor site and a piece of bone will be visualized on coronal or axial images. Rarely, the IGHL will rupture in its midsubstance, with discontinuity of the axillary recess on coronal images. Middle and superior glenohumeral ligament tears are uncommon. When present, they are best visualized on axial and sagittal MR arthrographic images. Posterior capsule injuries are also unusual but can occur with posterior dislocation.
Biceps Tendon Injury
B Figure 5-11. Superior labral anterior-posterior (SLAP) lesion. A, Coronal T2 fat-suppressed image. A linear high signal extends into the substance of the superior labrum (arrow). B, Coronal T1 fat-suppressed magnetic resonance arthrogram. Intra-articular contrast extends into the superior labral tear (arrow), increasing its conspicuity.
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Biceps tendinosis occurs when there is degeneration of the long head of the biceps caused by chronic microtrauma or acute injury.21 The tendon remains intact but may be thickened to greater than 5 mm in diameter. The patient typically complains of shoulder pain radiating into the upper arm, especially during overhead motion. This condition may be seen in conjunction with rotator cuff disease. MRI shows a thickened tendon on axial, coronal, or sagittal images, with increased T1 and T2 signals. The tendon of the long head of the biceps may also rupture, usually because of repetitive microtrauma.22 This
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Figure 5-12. Humeral avulsion of the glenohumeral ligament (HAGL) lesion; coronal T1 fat-suppressed magnetic resonance arthrogram. The inferior glenohumeral ligament (arrow) has been avulsed from its humeral attachment. Note the intra-articular contrast extending through the capsular defect.
Figure 5-13. Biceps tendon dislocation; axial T1 magnetic resonance arthrogram. A full-thickness tear of the subscapularis tendon (white arrow) has allowed medial dislocation of the biceps tendon (black arrow) into the anterior joint space. Note the empty bicipital groove.
condition often occurs with rotator cuff disease23 and bony encroachment from the acromioclavicular (AC) joint. The biceps muscle belly may retract distally, leading to the Popeye sign. A tear or gap in the tendon may be seen on MRI, with or without retraction. If there is significant retraction, the empty tendon sheath and bicipital groove will be identified on axial MR arthrographic images.
Primary extrinsic impingement occurs when the coracoacromial arch exerts pressure on the subacromial bursa and/or tendons of the rotator cuff, primarily the supraspinatus. The coracoacromial arch is composed of the following structures, from anterior to posterior: the coracoid process, the coracoacromial ligament, the distal clavicle, the AC joint, and the acromion. Impingement can occur at any of these locations (Fig. 5-14).27 Most commonly, there is hypertrophic degenerative change at the AC joint, producing capsular distention and distal clavicle osteophytes, both of which can extend inferiorly to encroach on the supraspinatus. The coracoacromial ligament may be thickened or produce traction on the acromion, resulting in a prominent anterior acromial spur (Fig. 5-15). The anterior acromial ossification center may fail to fuse, resulting in an os acromiale. If excessively mobile, the os acromiale can undergo inferior displacement with deltoid contraction.28 Other conditions, such as a type III acromion with an anterior hook, downsloping acromion, or low-lying acromion, can also produce encroachment on the cuff.29
Biceps tendon dislocation occurs after the loss of its stabilizing structures. The subscapularis tendon and coracohumeral ligament are the main stabilizers of the biceps tendon. A shallow bicipital groove also predisposes to dislocation. If the subscapularis tendon is intact, the dislocation is medial but on the same anterior plane as the bicipital groove.24 The tendon can dislocate medially and posteriorly all the way to the anterior labrum if the subscapularis tendon is torn (Fig. 5-13).25 MRI shows a round or oval low-signal structure outside the bicipital groove, which is left empty.
Shoulder Impingement and Rotator Cuff Abnormalities Evaluation of the rotator cuff is the most common indication for shoulder MRI. The power of MRI is its ability to answer many questions that the clinician may have regarding the status of the cuff. Not only can MRI accurately depict the status of the rotator cuff, but it can also demonstrate the potential underlying causative factors for the abnormality. Shoulder impingement is a clinical diagnosis made by clinicians. MRI can, however, provide important information to support this diagnosis.26,27
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Secondary extrinsic impingement is usually seen in athletes involved in throwing or overhead arm motion sports, such as baseball, football, tennis, or swimming. Such athletes are more susceptible to glenohumeral ligamentous instability. This instability can allow for superior migration of the humeral head during range of motion, producing impingement against the coracoacromial arch, which may appear anatomically normal.30 Internal impingement, or posterosuperior glenoid impingement, is another clinical entity associated with overhead
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AC Ac
to a rotator cuff abnormality, the posterosuperior glenoid labrum may suffer fraying or a discrete tear, and cystic changes may be found in the posterior humeral head.31 (Fig. 5-16) The use of the ABER position accentuates these abnormalities.32 The elbow is raised above the head with the hand positioned behind the head, resulting in
CI CA
Co
Figure 5-14. Coracoacromial arch; sagittal T1 magnetic resonance arthrogram. The coracoacromial arch is formed by the coracoid (Co), coracoacromial ligament (CA), distal clavicle (Cl), AC joint (AC), and acromion (Ac). An inferior distal clavicle osteophyte encroaches on the supraspinatus tendon (arrowhead).
A
Figure 5-15. Anterior acromial spur; sagittal T1 magnetic resonance arthrogram. Traction at the attachment of the coracoacromial ligament has produced a prominent spur (white arrow). Note the underlying tear of the supraspinatus tendon (black arrow).
sports. With the arm in the overhead position, the humerus is abducted and externally rotated. In this position, the undersurface of the supraspinatus and anterior infraspinatus may become entrapped between the greater tuberosity and the posterosuperior rim of the glenoid. In addition
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B Figure 5-16. Internal impingement. A, Coronal T2 fat-suppressed magnetic resonance arthrogram. In this baseball pitcher, there is increased signal in the supraspinatus tendon (arrow), with cystic change in the humeral head. B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. In the overhead position, there is interposition of the supraspinatus tendon (arrow) between the greater tuberosity and posterosuperior glenoid. A partial articular surface tear of the supraspinatus is revealed in this position.
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abduction and external rotation of the humerus. The ABER position approximates the overhead position responsible for this pathology. As a consequence of impingement, the subacromial bursa may become distended and inflamed. Visualization of more than a minimal amount of fluid in the bursa suggests subacromial bursitis. This fluid appears as high signal intensity on T2-weighted images. Fluid may extend into the subdeltoid bursa. Recent subacromial injection can also produce high signal in this location and should not be confused with bursitis. If possible, MRI should be performed before or at least 24 hours after subacromial injection to avoid confusion. A potential mimic of the impingement syndrome is calcific tendinitis. Any of the rotator cuff tendons may be involved, but the supraspinatus is the most commonly affected. In this condition, calcium hydroxyapatite deposition occurs in the tendon. The calcification may then extend into the subacromial or subdeltoid bursa or the glenohumeral joint. The calcification is usually best seen on radiographs; CT can be used in cases of very faint calcification. On MRI, calcification is low signal on all sequences. Distinguishing low-signal calcification from a low-signal tendon can sometimes be difficult. Ideally, shoulder MRI examinations should be interpreted with access to shoulder radiography. The calcification may be associated with edema within the tendon (tendinitis) or in the adjacent bursa (bursitis) (Fig. 5-17).
Figure 5-17. Calcific tendinitis; coronal T2 fat-suppressed magnetic resonance arthrogram. A globular low signal within the supraspinatus tendon (arrows) was confirmed on radiographs (not shown) as calcification. Note the small amount of fluid in the subacromial bursa and the edema in the supraspinatus muscle.
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Fluoroscopic or CT guidance can be used to aspirate the calcification in difficult cases. The tendons of the rotator cuff can undergo a spectrum of abnormalities, ranging from senescent degeneration to a full-thickness tear, with associated atrophy. Degenerative changes in the tendon are best described using the term tendinosis (or tendinopathy). Tendinitis is a clinical term with imaging features that overlap with those of tendinosis. The normal rotator cuff tendon is predominately low signal on all sequences. Tendinosis is seen as a mildly increased signal on T1-weighted or proton density (PD) sequences within the tendon, without the high signal on T2-weighted images that indicates fluid (Fig. 5-18).33 The tendon may be thickened. Tendinosis may or may not be seen in association with subacromial bursitis. Radiographic signs of rotator cuff tear are insensitive but include elevation of the humeral head, with decreased acromiohumeral distance. On standard MRI, a rotator cuff tear is identified by high T2 (bright) signal intensity within the tendon.26 There is usually some degree of underlying tendinosis unless a discrete traumatic event has occurred. With MR arthrography, contrast will enter any tear that communicates with the joint space. Partial-thickness tears of the rotator cuff may extend to the articular or bursal surface, or remain intrasubstance. Articular surface (or undersurface) tears are most common and tend to occur in one of two locations—the critical zone, which is about
Figure 5-18. Supraspinatus tendinosis; coronal T2 fat-suppressed magnetic resonance arthrogram. A mild increased signal is present in the supraspinatus tendon (arrow). No bright fluid signal intensity defect is present to suggest a tear. A very small amount of fluid is present in the subacromial bursa.
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1 cm proximal to the insertion onto the greater tuberosity, or at the attachment onto the tuberosity itself (Fig. 5-19). Contrast will extend into articular surface tears on MR arthrography, providing increased sensitivity over standard MRI. Bursal surface tears are often associated with subacromial bursitis (Fig. 5-20). Such tears are important to identify on MRI because they will not be visualized at arthroscopy. Pure intrasubstance tears of the cuff are uncommon; they are generally seen as extensions of an articular or bursal surface tear. Partial-thickness tears can be graded according to the percentage of the tendon thickness involved. Full-thickness tears of the rotator cuff are identified by discontinuity of tendon fibers extending from the articular to bursal surfaces. The tendon gap will exhibit high T2 signal throughout. On MR arthrography, contrast will extend from inside the joint through the tear into the subacromial or subdeltoid bursa (Fig. 5-21). Visualization of contrast in the bursa provides reliable evidence of a full-thickness defect in the tendon, again with increased sensitivity compared with standard MRI.34 In the setting of a rotator cuff tear on standard MRI, it can be difficult to determine whether fluid in the subacromial bursa is related to bursitis or extension of intra-articular fluid through a full-thickness defect. Absence of contrast in the subacromial bursa in this setting provides reassurance that the tear is not a full-thickness tear. Full-thickness tears may involve only a portion of the involved tendon or the tendon in its entirety (complete tear).
Figure 5-19. Partial tear supraspinatus tendon, articular surface; coronal T2 fat-suppressed magnetic resonance arthrogram. Focal high T2 signal is present in the distal supraspinatus tendon (arrow) at its attachment onto the greater tuberosity. The tear extends to the articular surface and involves 25% to 50% of the tendon thickness.
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Figure 5-20. Partial-thickness tear of the supraspinatus tendon, bursal surface; coronal T2 fat-suppressed magnetic resonance arthrogram. High T2 signal fills a bursal-sided partial tear (white arrow) of the supraspinatus tendon. The tear is associated with subacromial bursitis (black arrow).
Figure 5-21. Full-thickness tear of the supraspinatus tendon; coronal T1 fat-suppressed magnetic resonance arthrogram. Intra-articular contrast extends through a full-thickness tear of the supraspinatus tendon (arrow) into the subacromial bursa. Mild retraction of the tendon is present.
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The size of the tendon gap and degree of retraction of the tendon are important factors when operative repair is being considered. Another factor to consider is the acuity of the tear. Fatty atrophy of the rotator cuff muscle in question suggests a chronic process, with a corresponding decrease in likelihood of a satisfactory postoperative result. Massive rotator cuff tears involve two or more tendons (Fig. 5-22). These tears are seen in long-standing degenerative changes
85
in older patients or in cases of substantial trauma, usually in younger patients. The subscapularis tendon may be injured as a result of impingement or acute trauma, such as anterior shoulder dislocation. Full-thickness or even high-grade partialthickness tears of the subscapularis can allow for medial subluxation or dislocation of the biceps tendon out of the bicipital groove (see Fig. 5-13). The teres minor is rarely a source of clinical concern.
Muscle Injuries Pectoralis major musculotendinous abnormalities can present as anterior shoulder pain. The pectoralis major tendon inserts on the proximal humerus on the lateral lip of the intertubercular groove. The most common injuries of the pectoralis major are avulsion of the tendon at the bony attachment and partial tear at the musculotendinous junction.35,36 The degree of retraction, percentage of tendon involved, and status of the muscle can be assessed on MRI in a similar manner as with the rotator cuff (Fig. 5-23). The teres major and latissimus dorsi muscles are uncommon sources of shoulder pain. Strain is the most common injury involving these muscles (Fig. 5-24), although injury at the musculotendinous junction of the latissimus dorsi may occur.37 A
B Figure 5-22. Massive rotator cuff tear; coronal T1 fat-suppressed magnetic resonance arthrogram. A, There is a complete full-thickness tear of the supraspinatus tendon (arrow), with retraction to the level of the glenoid. B, A more posterior image shows that the infraspinatus tendon (arrow) is also completely torn and retracted.
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Figure 5-23. Pectoralis major tendon tear; axial T2-weighted image. There is a complete tear of the musculotendinous junction of the pectoralis major (black arrow), but the distal tendon attachment to the humerus (white arrow) remains intact.
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IS
Tm
TM
A
B
Figure 5-24. Muscle strains. A, Coronal proton density (PD) image. There is high signal throughout the teres major (TM) muscle. The infraspinatus (IS) and teres minor (Tm) muscles are labeled for reference. B, Axial T2 fat-suppressed image. High T2 signal and focal disruption of muscle fibers in the latissimus dorsi muscle (arrow) indicate strain, with a partial tear.
References 1. Magee T, Shapiro M, Williams D: Comparison of highfield-strength versus low-field-strength MRI of the shoulder. AJR Am J Roentgenol 181:1211-1215, 2003. 2. Neer CS: Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 52:1077-1089, 1970. 3. Kilcoyne RF, Shuman WP, Matsen FA 3rd, et al: The Neer classification of displaced proximal humeral fractures: spectrum of findings on plain radiographs and CT scans. AJR Am J Roentgenol 154:1029-1033, 1990. 4. Newberg AH: Computed tomography of joint injuries. Radiol Clin North Am 28:445-460, 1990. 5. Potter HG, Foo LF: Magnetic resonance imaging of articular cartilage: Trauma, degeneration, and repair. Am J Sports Med 34:661-677, 2006. 6. Steinbach LS, Palmer WE, Schweitzer ME: Special focus session. MR arthrography. Radiographics 22:1223-1246, 2002. 7. Emig EW, Schweitzer ME, Karasick D, Lubowitz J: Adhesive capsulitis of the shoulder: MR diagnosis. AJR Am J Roentgenol 164:1457-1459, 1995. 8. Connell D, Padmanabhan R, Buchbinder R: Adhesive capsulitis: Role of MR imaging in differential diagnosis. Eur Radiol 12:2100-2106, 2002. 9. Connor PM, Banks DM, Tyson AB, et al: Magnetic resonance imaging of the asymptomatic shoulder of overhead athletes: A 5-year follow-up study. Am J Sports Med 31:724-727, 2003. 10. De Maeseneer M, Jaovisidha S, Jacobson JA, et al: The Bennett lesion of the shoulder. J Comput Assist Tomogr 22: 31-34, 1998.
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11. Ferrari JD, Ferrari DA, Coumas J, Pappas AM: Posterior ossification of the shoulder: The Bennett lesion. Etiology, diagnosis, and treatment. Am J Sports Med 22:171-175, 1994. 12. Matheson GO: Evaluating the dislocated shoulder joint with MRI and arthroscopy. Clin J Sport Med 14:148-151, 2004. 13. Cvitanic O, Tirman PF, Feller JF, et al: Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. AJR Am J Roentgenol 169: 837-844, 1997. 14. Wischer TK, Bredella MA, Genant HK, et al: Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenol 178:233-237, 2002. 15. Waldt S, Burkart A, Imhoff AB, et al: Anterior shoulder instability: Accuracy of MR arthrography in the classification of anteroinferior labroligamentous injuries. Radiology 237:578-583, 2005. 16. Harper KW, Helms CA, Haystead CM, Higgins LD: Glenoid dysplasia: Incidence and association with posterior labral tears as evaluated on MRI. AJR Am J Roentgenol 184: 984-988, 2005. 17. Tuite MJ, Rutkowski A, Enright T, et al: Width of high signal and extension posterior to biceps tendon as signs of superior labrum anterior to posterior tears on MRI and MR arthrography. AJR Am J Roentgenol 185:1422-1428, 2005. 18. Tung GA, Entzian D, Stern JB, Green A: MR imaging and MR arthrography of paraglenoid labral cysts. AJR Am J Roentgenol 174:1707-1715, 2000.
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19. Takubo Y, Horii M, Kurokawa M, et al: Magnetic resonance imaging evaluation of the inferior glenohumeral ligament: Non-arthrographic imaging in abduction and external rotation. J Shoulder Elbow Surg 14:511-515, 2005. 20. Chung CB, Sorenson S, Dwek JR, Resnick D: Humeral avulsion of the posterior band of the inferior glenohumeral ligament: MR arthrography and clinical correlation in 17 patients. AJR Am J Roentgenol 183:355-359, 2004. 21. Patton WC, McCluskey GM 3rd; Biceps tendinitis and subluxation. Clin Sports Med 20:505-529, 2001. 22. Zanetti M, Weishaupt D, Gerber C, Hodler J: Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: Evaluation with MR arthrography. AJR Am J Roentgenol 170:1557-1561, 1998. 23. Beall DP, Williamson EE, Ly JQ, et al: Association of biceps tendon tears with rotator cuff abnormalities: Degree of correlation with tears of the anterior and superior portions of the rotator cuff. AJR Am J Roentgenol 180:633-639, 2003. 24. Cervilla V, Schweitzer ME, Ho C, et al: Medial dislocation of the biceps brachii tendon: Appearance at MR imaging. Radiology 180:523-526, 1991. 25. Chan TW, Dalinka MK, Kneeland JB, Chervrot A: Biceps tendon dislocation: Evaluation with MR imaging. Radiology 179:649-652, 1991. 26. Reinus WR, Shady KL, Mirowitz SA, Totty WG: MR diagnosis of rotator cuff tears of the shoulder: Value of using T2-weighted fat-saturated images. AJR Am J Roentgenol 164:1451-1455, 1995. 27. Seeger LL, Gold RH, Bassett LW, Ellman H: Shoulder impingement syndrome: MR findings in 53 shoulders. AJR Am J Roentgenol 150:343-347, 1988. 28. Park JG, Lee JK, Phelps CT: Os acromiale associated with rotator cuff impingement: MR imaging of the shoulder. Radiology 193:255-257, 1994.
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29. Peh WC, Farmer TH, Totty WG: Acromial arch shape: Assessment with MR imaging. Radiology 195:501-505, 1995. 30. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-975, 1989. 31. Giaroli EL, Major NM, Higgins LD: MRI of internal impingement of the shoulder. AJR Am J Roentgenol 185: 925-929, 2005. 32. Roger B, Skaf A, Hooper AW, et al: Imaging findings in the dominant shoulder of throwing athletes: Comparison of radiography, arthrography, CT arthrography, and MR arthrography with arthroscopic correlation. AJR Am J Roentgenol 172:1371-1380, 1999. 33. Kjellin I, Ho CP, Cervilla V, et al: Alterations in the supraspinatus tendon at MR imaging: Correlation with histopathologic findings in cadavers. Radiology 181:837-841, 1991. 34. Ferrari FS, Governi S, Burresi F, et al: Supraspinatus tendon tears: Comparison of US and MR arthrography with surgical correlation. Eur Radiol 12:1211-1217, 2002. 35. Lee J, Brookenthal KR, Ramsey ML, et al: MR imaging assessment of the pectoralis major myotendinous unit: An MR imaging-anatomic correlative study with surgical correlation. AJR Am J Roentgenol 174:1371-1375, 2000. 36. Connell DA, Potter HG, Sherman MF, Wickiewicz TL: Injuries of the pectoralis major muscle: Evaluation with MR imaging. Radiology 210:785-791, 1999. 37. Schickendantz MS, Ho CP, Keppler L, Shaw BD: MR imaging of the thrower’s shoulder. Internal impingement, latissimus dorsi/subscapularis strains, and related injuries. Magn Reson Imaging Clin North Am 7:39-49, 1999.
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CHAPTER 6 Normal Arthroscopic Anatomy
of the Shoulder William G. Carson, Jr. and Scott B. Reynolds
Diagnostic and operative arthroscopy of the shoulder has been well established for the treatment of various shoulder disorders.1-18 Diagnostic and surgical techniques, as well as the arthroscopic anatomy of the shoulder, have been well described.3,5,7,9,14,19-27 Surgical techniques include glenoid labrum resections,2,11,15 certain rotator cuff débridements, and impingement releases,1,28-33 for the débridement of a degenerative shoulder17 or for the resection of a degenerative acromioclavicular joint.16,18 Arthroscopic techniques have also been developed for arthroscopic Bankart repairs34,35 and for arthroscopic staple capsulorrhaphy of the shoulder for recurrent anterior instability.36-40 Additionally, techniques for superior labral anterior-posterior (SLAP) repairs,41 posterior labral repairs,42 and rotator cuff repairs43,44 have also been developed. Techniques to address other forms of shoulder pathology are continuing to be delineated. A knowledge of the normal anatomy of the shoulder as viewed arthroscopically is an essential prerequisite for orthopedic surgeons performing any of these surgical procedures. This section describes the normal arthroscopic anatomy of the shoulder.
from an imaginary vertical line. It attaches to the supraglenoid tubercle at the posterosuperior aspect of the glenoid and, in this area, is related to and appears to be continuous with the glenoid labrum (Fig. 6-3). This attachment of the biceps tendon at the superior labrum is involved in the SLAP lesions commonly seen in overhead throwing athletes. The patient’s arm can be externally rotated to facilitate visualization of the biceps tendon, which can be followed anteriorly to portions of the bicipital groove. The normal biceps tendon should appear glistening and smooth and free of any adhesions, fraying, synovitis, or partial tearing.
Humeral Head and Glenoid After inspection of the biceps tendon is complete and proper orientation is once again obtained, the articular surfaces of the humeral head (superiorly) and the glenoid (inferiorly) are examined. Both these articular surfaces are covered by hyaline cartilage. With the patient positioned in the lateral decubitus position, approximately one third of the articular surface of the humeral head can be seen, which is oriented in 30 degrees of retroversion. Examination of the entire articular surface of the humeral head is facilitated by rotating the arthroscope superiorly and moving the humeral head into internal and external rotation. Anteriorly, the articular surface of the humeral head extends to the level of the humeral neck and is near the insertion of the subscapularis. However, there can be variations in the humeral head’s articular surface extension posteriorly to the soft tissues. Posteriorly, the rotator cuff attaches lateral to the actual extent of the articular cartilage, and thus a bare area of bone can be visualized. This bare area is located, for the most part, straight posteriorly and should not be confused with the Hill-Sachs lesion, which is located more posterolaterally. The size of the normal bare area can vary, but this normal area is usually smooth and rounded without evidence of fraying or degeneration, indicative of possible trauma. Also, the bare area is often characterized by different blood vessels that can be seen coursing through it.
STRUCTURAL ANATOMIC CONSIDERATIONS The arthroscopic anatomy and its various relationships, as shown in the figures for this chapter, are representative of those seen with the patient in the lateral decubitus position, with the shoulder superior. The arm is abducted approximately 45 degrees and forward flexed 15 degrees.3-5,23 Most of the photographs and illustrations represent a posterior portal, which is the preferred approach for diagnostic arthroscopy of the shoulder. This posterior portal is located approximately 3 cm inferior to and slightly medial to the posterolateral corner of the acromion (Fig. 6-1). This point corresponds to the soft spot on the posterior aspect of the shoulder that comprises the relative interval between the infraspinatus and teres minor muscles (Fig. 6-2).
Biceps Tendon
The glenoid is a bean- or pear-shaped cavity approximately one fourth the size of the humeral head. Its surface is longer in the superior-to-inferior dimension than in the anterior-to-posterior dimension. The articular surface clinically appears to be thicker near its periphery than in its central portions.
The long head of the biceps tendon is usually the first structure identified after the arthroscope has been inserted into the shoulder through a posterior portal. This provides proper orientation and, with the patient positioned in the lateral decubitus position, the long head of the biceps tendon is oriented approximately 10 to 15 degrees away 91
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Glenoid Labrum The glenoid labrum is a wedge-shaped structure that borders the glenoid cavity and appears to provide inherent stability to the glenohumeral joint, thus restricting anterior and posterior excursion of the humerus (see Fig. 6-3).45,46 The glenoid labrum consists of hyaline cartilage, fibrocartilage, and fibrous tissue.45-51 This fibrocartilaginous rim of tissue surrounds the glenoid circumferentially and portions of the labrum appear to overlap the articular surface of the glenoid or articular surface. This overlap portion of the glenoid labrum appears to deepen the glenoid, providing some inherent stability to the glenohumeral joint, primarily by restricting anterior excursion. The glenoid surface of the labrum is continuous with the hyaline cartilage of the glenoid cavity, whereas the capsular surface blends with the joint capsule and glenohumeral ligaments. There can be variations in the width or thickness of the glenoid labrum, particularly at the different locations of the glenoid as it relates to the glenoid rim. Thus, the anterior glenoid may appear to be thicker than the posterior aspect of the glenoid labrum in some individuals. At times, particularly anteriorly, the glenoid labrum can appear to be large and almost hypermobile; occasionally it appears to be analogous to a meniscus that can be seen arthroscopically in the knee joint. At other times, the glenoid labrum can be smaller and appears to be more firmly attached to the edge of the glenoid and to blend more with the actual hyaline cartilage surface. One common anatomic variant of the anterior labrum is the Buford complex, which involves a cordlike middle glenohumeral ligament that attaches to the superior labrum; also, the anterior labrum above the midglenoid notch is absent.52
Figure 6-1. Arthroscope in place through a posterior portal in a right shoulder.
B A
The normal glenoid labrum should appear to be smooth and lack any fraying, partial tearing, or excessive hypermobility. The usual inspection of the glenoid begins at the insertion of the biceps tendon, which appears to insert through the superior portion of the labrum into the supraglenoid tubercle. With traction placed on the arm with the traction apparatus, portions of the inferior glenoid rim can be visualized. Slight retraction and posterior rotation
Figure 6-2. Relative interval between infraspinatus and teres minor muscles. This cadaveric specimen shows the relative interval between the infraspinatus (A) and teres minor (B) muscles traversed by the arthroscope when establishing a posterior portal.
B Figure 6-3. Biceps tendon and other structures. A, Arthroscopic view of a right shoulder with the patient in lateral decubitus position and the arm abducted 45 degrees. Structures that can be identified are the long head of the biceps tendon (A), superior glenohumeral ligament (B), anterior portion of the glenoid labrum (C), and humeral head (D). B, Biceps tendon is oriented in a vertical direction (A). The supraspinatus portion of the rotator cuff (B) is just superior and intimately related to the biceps tendon in this view.
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D B A
A C
A
B
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of the arthroscope will allow examination of the posterior rim of the glenoid labrum from a posterior arthroscopic portal. The arthroscope can be changed to an anterior portal for better visualization of the more posterior portions of the glenoid rim.
Glenohumeral Ligaments The terms superior, middle, and inferior glenohumeral ligaments are used to describe the different thickenings of the anterior and inferior capsule of the shoulder joint. These glenohumeral ligaments are not free-standing distinct ligaments that can be seen, for example, in the ankle or the knee joint; they simply represent the different portions or thickenings of the capsule of the shoulder. There can be much variation in the thickness or presence of the superior, middle, and inferior glenohumeral ligaments. These glenohumeral ligaments stabilize the anterior and inferior portions of the shoulder capsule.47,50,53-56 When viewed arthroscopically, the glenohumeral ligaments are displaced anteriorly because of fluid distention within the shoulder joint. In actuality, these ligaments normally lie closer to the glenoid labrum (Fig. 6-4). Occasionally, they will be seen to have distinct labral origins rather than their usual capsular origins originating off the edge of the glenoid labrum. The superior glenohumeral ligament, together with the coracohumeral ligament, stabilizes the shoulder joint when the arm is in the abducted dependent position.50,53 This ligament has two proximal attachments—one to the superior aspect of the labrum conjoined with the biceps tendon and one to the
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base of the coracoid.56 This ligament courses laterally to insert on the anterior aspect of the anatomic neck of the humerus. The superior glenohumeral ligament can occasionally be seen near the insertion of the biceps tendon into the superior aspect of the glenoid; however, it may be hidden behind the biceps tendon or may appear to be absent. The middle glenohumeral ligament stabilizes the glenohumeral joint when the shoulder is abducted 45 degrees.56 Although the attachments of this ligament are wide, they may be difficult to visualize arthroscopically. However, the middle portion of the ligament can usually be seen just posterior to the subscapularis tendon, with which it occasionally appears to fuse. The middle glenohumeral ligament extends from just beneath the superior glenohumeral ligament, along the anterior border of the glenoid, to the junction of the middle and inferior third of the glenoid rim, except in cases of a Buford complex, as previously described. It blends with the capsule of the anteroinferior aspect of the shoulder joint and inserts near the lesser tuberosity over the anterior aspect of the anatomic neck of the humerus. The inferior glenohumeral ligament consists of an anterior and posterior band. The anterior band provides stability when the arm is abducted and externally rotated, whereas the posterior band stabilizes the shoulder in abduction and internal rotation.57 This triangular ligament arises from the anteroinferior and posteroinferior margins of the glenoid and inserts into the inferior aspect of the surgical neck of the humerus. Both the anterior and posterior bands can be seen arthroscopically when the arm is in abduction.
Subscapularis Tendon and Recess
C
A
D
E
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Figure 6-4. Intra-articular structures that can be visualized arthroscopically in a right shoulder. These include the long head of the biceps tendon (A), superior glenohumeral ligament (B), subscapularis tendon (C), middle glenohumeral ligament (D), and inferior glenohumeral ligament (E).
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With the arm in the abducted position, the posterosuperior aspect of the subscapularis tendon can be seen over the anterior aspect of the shoulder between the superior and middle glenohumeral ligaments (Fig. 6-5). At times, however, the subscapularis tendon may be obscured by or appear to blend with the middle glenohumeral ligament. When viewed in most anatomy textbooks or when viewed grossly at the time of open or arthrotomy surgery to the shoulder, the subscapularis muscle and tendon usually appear to be a broad flat structure extending from the more medial aspects of the anterior aspect of the scapula to insert onto the lesser tuberosity of the humerus. However, at the time of arthroscopic surgery, with the patient’s arm abducted approximately 45 degrees, and when viewed from a posterior arthroscopic portal, only the posterosuperior edge of the tendon can be seen, which now appears to be a distinct ropelike banded structure, different from that normally seen in anatomy textbooks (Fig. 6-6). The subscapularis recess is found over the anterior aspect of the shoulder in the area of the middle glenohumeral ligament. There can be much variation in the appearance of the relationship of the middle glenohumeral ligament to the recess, which occasionally can appear to be absent.
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A A B Figure 6-5. Posterosuperior aspect of the subscapularis tendon. A, Subscapularis tendon (A), middle glenohumeral ligament (B), and anterior aspect of glenoid labrum (C) in a right shoulder. B, Arthroscopic view of subscapularis tendon (A) and middle glenohumeral ligament (B) in a right shoulder.
B C
A
Rotator Cuff Arthroscopic evaluation of the rotator cuff begins by identifying the biceps tendon and obtaining proper orientation. The supraspinatus portion of the rotator cuff can be seen just superior to the biceps tendon (Fig. 6-7A). To visualize the more posterior portions of the rotator cuff, the arthroscope is
B
retracted and directed superiorly and slightly posteriorly to reveal the insertion of the tendinous portion of the infraspinatus and teres minor into the humeral head (see Fig. 6-7B). Arthroscopically, the more posterior portions of the rotator cuff inserting into the humeral head and moving toward the glenoid surface are visualized, the posterior portions of the rotator cuff appear to blend with the posterior capsule. The rotator cuff should be one continuous structure and free of any partial tears, complete tears, or fraying. The attachment of the rotator cuff should be firm, and no bone should be visualized beneath the insertion site.
A
B
When viewed arthroscopically, the articular surface of an intact rotator cuff will have an arching cable-like thickening of the capsule surrounding a thinner crescent of tissue that inserts on the greater tuberosity.58,59 This cable-like structure extends from the biceps to the inferior margin of the infraspinatus, spanning the supraspinatus and infraspinatus insertions at the avascular zone margin. The rotator cable potentially serves a protective role, allowing stress to be transferred along the cable and thereby protecting the thinner, avascular, crescent tissue attachment of the cuff.
Rotator Interval The rotator interval is the space between the supraspinatus and subscapular tendons. This interval is easily identified arthroscopically while viewing the posterior portal. During arthroscopy, the interval is defined as the triangular space outlined by the anterior edge of the supraspinatus tendon, superior edge of the subscapularis tendon, and anterior rim of the glenoid. This space is the location of the standard anterior portal. Plication of this interval is sometimes done while treating certain types of instability patterns.60
Superior Recess and Subacromial Space Figure 6-6. Posterosuperior edge of subscapularis tendon and biceps tendon. This cadaveric specimen shows the posterosuperior edge of the subscapularis tendon (A) and biceps tendon (B) when viewed from a posterior arthroscopic portal.
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The superior recess is located superior to and slightly anterior to the superior aspect of the glenoid and to the insertion of the biceps tendon (Fig. 6-8).
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B
A
A
A
B
Figure 6-7. Rotator cuff. A, Arthroscopic view of the biceps tendon (A) and supraspinatus portion of the rotator cuff (B) in a right shoulder. B, Arthroscopic view of the more posterior portions of the rotator cuff (infraspinatus and teres minor) in a right shoulder (A).
The subacromial space, or subacromial bursa, is the area inferior to the distal clavicle, acromioclavicular joint, and acromion and superior to the humeral head and rotator cuff. This subacromial space is bordered superiorly by the subacromial arch that consists of the undersurface of the acromion, outer end of the clavicle, acromioclavicular joint, and coracoacromial ligament, which forms a fibrous roof. The base of the subacromial space is the greater tuberosity of the humerus and the insertion of the rotator cuff. The subacromial bursa forms the actual joint cavity (Fig. 6-9). The subacromial bursa attaches superiorly to the undersurface of the acromion and below to the greater tuberosity at the insertion of the rotator cuff tendons.61 Arthroscopic visualization of the subacromial bursa is sometimes difficult; many clinicians believe that visualization of this subacromial bursa should always be difficult if the
patient has an impingement syndrome29 or other pathology in the subacromial space. If a normal-appearing bursa is seen, the patient’s problems are probably not related to the subacromial space nor to an impingement problem. Structures that should be visualized in the subacromial space are the inferior surface of the acromion, the acromioclavicular joint, the superior portion of the coracoacromial ligament, the superior surface of the rotator cuff, and the bursa itself. On entering the subacromial bursa through a posterior portal, a bursal curtain or sheet is often encountered, which can make visualization difficult (Fig. 6-10). The arthroscope has to be passed well anterior to this bursa shelf for the actual subacromial space itself to be visualized. Once in the subacromial space, it is possible to identify the inferior surface of the acromion, which is covered by periosteum and extended fibers from the coracoacromial ligament and
C
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E
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Figure 6-8. Superior recess. This is located just above the biceps tendon insertion or to the left of the biceps tendon (A) in this arthroscopic view of a right shoulder.
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Figure 6-9. Subacromial space structures. These include the bursa (A), rotator cuff (B), acromion (C), coracoacromial ligament (D), and acromioclavicular joint (E).
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B A
A
Figure 6-12. Superior surface of the rotator cuff. This arthroscopic subacromial space visualization shows the superior surface of the rotator cuff (A) in a right shoulder. Figure 6-10. Arthroscopic view of bursal shelf or curtain. The bursal shelf (A) is normally seen on visualization of the subacromial space (B) in a right shoulder.
therefore has a softer appearance as compared with a bony appearance. Also, it is possible to visualize clearly the superior portion of the coracoacromial ligament (Fig. 6-11). The superior surface of the rotator cuff should be inspected carefully for any evidence of partial tearing or full-thickness tears and should have a smooth homogenous appearance (Fig. 6-12). Portions of the inferior surface of the acromioclavicular joint can usually be visualized arthroscopically. However, it
may be obscured by a large fat pad covering the inferior surface of this joint. The subacromial bursa is a reasonably large space, and in the absence of any pathologic processes, most structures described can be viewed arthroscopically. In the presence of pathologic processes such as subacromial bursitis or inflammation, or with partial or complete rotator cuff tears, the subacromial space at times can be almost obliterated by hypertrophic bursal tissue. In such cases, visualization is almost impossible until a space is created, with the motorized instrumentation performed arthroscopically.
SUMMARY
B A
Diagnostic and operative arthroscopy of the shoulder is a reasonably demanding surgical procedure. Attention to detail is required to perform a safe, reproducible, and systematic arthroscopic evaluation. The structures described in this chapter should be visualized on each arthroscopic evaluation of the shoulder, which should be performed systematically to ensure an accurate and reproducible examination.
References
Figure 6-11. Superior portion of the coracoacromial ligament. This arthroscopic subacromial space visualization shows the inferior surface of the acromion (A) and superior edge of coracoacromial ligament (B) in a right shoulder.
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1. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117, 1985. 2. Andrews JR, Carson WG, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. 3. Andrews JR, Carson WG: Shoulder joint arthroscopy. Orthopedics 6:1157, 1983.
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4. Andrews JR, Carson WG: Operative arthroscopy of the shoulder in the throwing athlete. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, p 84. 5. Andrews JR, Carson WG: Arthroscopic surgery of the shoulder. In Parisien JS (ed): Arthroscopic Surgery. New York, McGraw-Hill, 1987, p 231. 6. Gross RM, Fitzgibbons TC: Shoulder arthroscopy: A modified approach. Arthroscopy 1:156, 1985. 7. Neviarser TJ: Arthroscopy of the shoulder. Orthop Clin North Am 18:361, 1987. 8. Ogilvie-Harris DJ, Wiley AM: Arthroscopic surgery of the shoulder. J Bone Joint Surg Br 68:201, 1986. 9. Johnson LL: Shoulder arthroscopy. In Johnson LL (ed): Arthroscopic Surgery. St. Louis, Mosby, 1986, p 1301. 10. McFlynn FJ, Caspari RB: Arthroscopic findings in the subluxing shoulder. Clin Orthop 183:173, 1984. 11. Snyder SJ, Kargel RP, DelPizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274, 1990. 12. Wheeler JH, Ryan JB, Arciero RA, Moliman RN: Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy 5:213, 1989. 13. Buss DD, Warren RF, Galinat BJ: Indications for shoulder arthroscopy. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 465. 14. Andrews JR, Heckman MM: Shoulder arthroscopy, operating room set-up. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 473. 15. Snyder SJ, Ramer RD, Walbert E: Labral lesions. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 491. 16. Meyers JF: Arthroscopic debridement of the acromioclavicular joint and distal clavicle resection. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 557. 17. Matthews LS, Wolock BS, Martin DF: Arthroscopic management of degenerative arthritis of the shoulder. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 567. 18. Gartsman GM, Combs AH, Davis PF, Tullos HS: Arthroscopic acromioclavicular joint resection. An anatomical study. Am J Sports Med 19:2, 1991. 19. Andrews JR, Carson WG, Ortega K: Arthroscopy of the shoulder: Technique and normal anatomy. Am J Sports Med 12:1, 1984. 20. Matthews LS, Zarins B, Michael RH, Helfet DL: Anterior portal selection for shoulder arthroscopy. Arthroscopy 1:33, 1985. 21. Carson WG: Arthroscopy of the shoulder: Normal anatomy. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, p 83. 22. Wolf EM: Anterior portals for shoulder arthroscopy. Arthroscopy 5:201, 1989. 23. Andrews JR, Carson WG: Arthroscopic anatomy of the shoulder. Shoulder surgery in the athlete. In Jackson DW (ed): Techniques in Orthopaedics. Rockville, Md, Aspen Systems, 1985, p 25. 24. Blanchut PA, Day B: Arthroscopic anatomy of the shoulder. Arthroscopy 5:1, 1989. 25. Matthews LS, Fadale PD: Subacromial anatomy for the arthroscopist. Arthroscopy 5:36, 1989. 26. Arnoczky SP, Altchek DW, O’Brien SJ: Anatomy of the shoulder. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 425.
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27. Souryal TO, Baker CL: Anatomy of the supraclavicular fossa portal in shoulder arthroscopy. Arthroscopy 6:297, 1990. 28. Ellman H: Arthroscopic subacromial decompression. Analysis of one- to three-year results. Arthroscopy 3:173, 1987. 29. Ellman H: Arthroscopic acromioplasty. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 543. 30. Snyder SJ, Pachelli AF, DelPizzo W et al: Partial-thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1, 1991. 31. Levy HJ, Uribe JW, Delaney LG: Arthroscopic-assisted rotator cuff repair: Preliminary result. Arthroscopy 6:55, 1990. 32. Paulos LE, Franklin JL, Beck CL: Arthroscopic management of rotator cuff tears. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 529. 33. Levy JH, Gardner RD, Lemak LJ: Arthroscopic subacromial decompression in the treatment of full thickness rotator cuff tears. Arthroscopy 7:8, 1991. 34. Caspari RB, Savoie FH: Arthroscopic reconstructions of the shoulder: The Bankart repair. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 507. 35. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111, 1987. 36. Hawkins RB: Arthroscopic stapling repair for shoulder instability: A retrospective study of 50 cases. Arthroscopy 5:122, 1989. 37. Detrisac DA: Arthroscopic shoulder staple capsulorrhaphy for traumatic anterior instability. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 517. 38. Matthews LS, Vetter WL, Oweida SJ, et al: Arthroscopic staple capsulorrhaphy for recurrent anterior shoulder instability. Arthroscopy 4:106, 1988. 39. Wiley AM: Arthroscopy for shoulder instability and a technique for arthroscopic repair. Arthroscopy 4:25, 1988. 40. Matthews LS, Helfet DL, Spearman J, Oweida S: Arthroscopic staple capsulorrhaphy for anterior instability of the shoulder. Arthroscopy 2:116, 1986. 41. Burkhart SS, Morgan C: SLAP lesions in the overhead athlete. Orthop Clin North Am 32:431, 2001. 42. Goubier JN, Iserin A, Augereau B: The posterolateral portal: A new approach for shoulder arthroscopy. Arthroscopy 17:1000, 2001. 43. Cole BJ, El Attrache NS, Anbari A: Arthroscopic rotator cuff repairs: An anatomic and biomechanical rationale for different suture–anchor repair configurations. Arthroscopy 23:662, 2007. 44. Burkhart SS: A stepwise approach to arthroscopic rotator cuff repair based on biomechanical principals. Arthroscopy 16:82, 2000. 45. Bankart ASB: The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 26:23, 1938. 46. DePalma AF: Surgery of the Shoulder. Philadelphia, JB Lippincott, 1973. 47. Bost FC, Inman VT: The pathological changes in recurrent dislocation of the shoulder. A report of Bankart’s operative procedure. J Bone Joint Surg Am 24:595, 1942. 48. Dutoit GT, Roux D: Recurrent dislocation of the shoulder. A twenty-four year study of the Johannesburg stapling operation. J Bone Joint Surg Am 38:1, 1956. 49. Warwick R, Williams P (eds): Gray’s Anatomy of the Human Body. Philadelphia, WB Saunders, 1973. 50. Mosely JF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913, 1962.
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51. Rowe CR, Patell D, Southmayd WW: The Bankart procedure. a long-term, end-results study. J Bone Joint Surg Am 60:1, 1978. 52. Williams MM, Snyder SJ, Buford D Jr.: The Buford complex: The cord-like middle glenohumeral ligament and absent anterosuperior labrum complex: A normal anatomic capsulolabral variant. Arthroscopy 10:241, 1994. 53. Basmajian JV, Bazant FJ: Factors preventing downward dislocation of the adducted shoulder. J Bone Joint Surg Am 41:1182, 1959. 54. Rowe DR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863, 1981. 55. Schlemm F: Über die verstarkungsbander am schultergelenk. Arch Anat 45, 1853. 56. Turkel SJ, Panio MW, Marshall JL, et al: Stabilizing mechanism preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208, 1981.
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57. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298, 1995. 58. Clark JM, Harryman DT II: Tendons, ligaments, and capsule of the rotator cuff. J Bone Joint Surg Am 74:713, 1992. 59. Burkhart SS, Esch JC, Jolson RC: The rotator crescent and rotator cable: An anatomic description of the shoulder’s “suspension bridge.” Arthroscopy 9:611,1993. 60. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557, 1995. 61. Ellman H: Arthroscopic subacromial decompression. In Parisien JS (ed): Arthroscopic Surgery. New York, McGraw-Hill, 1988, p 243.
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CHAPTER 7 Operative Arthroscopy of the Shoulder Scott B. Reynolds, Joe P. Bramhall, Dorothy F. Scarpinato, and James R. Andrews
Understanding the management of the athlete’s shoulder has been difficult and controversial. With the different technological advances and convergence of ideas from orthopedic surgeons who perform shoulder surgery, a better understanding of the pathology and treatment is continuing to evolve. Surgical treatment, in general, should be as conservative as possible. Operative arthroscopy has its role, especially after conservative treatment fails. For other more severe cases, open operative intervention still has a place in the treatment armamentarium.
8 mm of the anterior acromion, extending medially to the acromioclavicular joint and beveled posteriorly for about 2 cm. This is a technically demanding procedure, and care should be taken to control bleeding.
This section addresses special considerations for the indications and contraindications for arthroscopic examination of the athlete’s shoulder and its use for treatment of the throwing athlete’s shoulder. The actual recognition and treatment of each of these pathologies are addressed in other chapters in this text.
Arthroscopic decompression of the subacromial space has minimal morbidity because the insertion of the deltoid is not violated.4 It also allows for early rehabilitation, which in turn allows for an earlier return to competition.
If there is partial tearing of the superior surface of the rotator cuff, this may be débrided to healthy bleeding tissue or repaired. At this time, the humeral head is rotated to assess the adequacy of the amount of space available between the acromion and rotator cuff.
Secondary Compressive Cuff Disease Impingement may be secondary to another underlying problem, such as glenohumeral instability.4 The correct diagnosis is mandatory, because treatment includes alleviating the primary problem. The patient may present only with a complaint of pain; therefore, a thorough history and physical examination must be performed. Emphasis should be placed on comparing range of motion and anteriorposterior translation of the humeral head to the opposite shoulder. Generalized ligamentous laxity should be noted. A special test that is helpful to determine anterior capsular laxity is Lachman’s test of the shoulder, which is similar to Lachman’s test of the knee for anterior cruciate ligament laxity. With the patient supine and the shoulder abducted 90 degrees and externally rotated about 45 degrees, an anterior force is applied to the humeral head to assess the anterior translation of the glenohumeral joint and end point of the anterior capsule.
COMPRESSIVE CUFF DISEASE Primary Compressive Cuff Disease Primary compressive cuff disease can be a primary cause for cuff disease when associated with a type III hooked acromion,1 degenerative spurs, os acromiale or, in some cases, a congenitally thickened coracoacromial ligament. It can also be caused by the prominence of a degenerated acromioclavicular joint. Compressive cuff disease results in an outside-in type of rotator cuff tear. Overhead sports movements that require using the arm in a 90-degree or greater horizontally abducted position, with rotation into internal and horizontal adduction, are likely to produce impingement symptoms. These are reproducible on physical examination by forceful forward flexion (positive impingement sign).2 Pain relief by injecting 1% lidocaine into the subacromial space helps confirm the diagnosis. Most patients respond to a conservative program of active rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and progressive rotator cuff strengthening and stretching exercises.3
If anterior laxity is evident, the compressive cuff disease may be secondary to anterior shoulder laxity. If only mild instability is present, treatment options in this situation include rehabilitation, with an emphasis on dynamic stabilization by muscular strengthening. If this fails, arthroscopic or open stabilization may be warranted. Primary rotator cuff failure from tensile overload may also cause secondary impingement. This failure occurs because of repetitive tensile overloading of the cuff, as is seen in the deceleration phase of throwing. These forces encountered in athletic activity may ultimately exceed the ability
If the athlete’s symptoms are not relieved by nonoperative measures, surgical treatment may be warranted. Arthroscopy of the subacromial space may reveal bursitis that can be easily débrided with a motorized resector. An acromioplasty is performed using a motorized burr, removing approximately 99
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of the dynamic stabilizers and anterior static stabilizers of the rotator cuff to compensate, which may lead to a secondary impingement phenomenon of the rotator cuff.4 Again, rehabilitation may be the first line of treatment; if this fails, arthroscopic débridement of the tensile tear is performed, along with anterior stabilization, decompression of the coracoacromial arch, or both, as necassary.
INTERNAL IMPINGEMENT Internal impingement is a concept that has developed as our understanding of the thrower’s shoulder has evolved. Walch and colleagues5 had initially described pinching of the posterosuperior rotator cuff between the posterosuperior glenoid labrum and greater tuberosity as the arm is abducted and externally rotated. Jobe6 has hypothesized that internal impingement is exacerbated in overhead throwing athletes with anterior microinstability. Burkhart and associates7 have emphasized that type II superior labral anterior-posterior (SLAP) lesions are a major pathology associated with the symptoms of internal impingement. The arthroscopic findings associated with internal impingement include a combination of injuries involving partial-thickness, articular-sided, rotator cuff tears in the posterior supraspinatus and anterior infraspinatus.8-10 There is also typical pathology of the posterior superior labrum and changes on the posterior humeral head, including an expanded bare area and cyst formation.5,6,11 In addition, most shoulders are believed to have a component of anterior microinstability, 6,12,13 which worsens the internal impingement, or a tight posteroinferior capsule,7 resulting in posterosuperior glenohumeral translation and anteroinferior pseudolaxity. The implications and treatment of these findings will be discussed in further detail in later chapters.
TENSILE LESIONS
rotation weakness from the abducted position. Magnetic resonance imaging may reveal a partial undersurface tear of the rotator cuff. Initially, the athlete is started on a rehabilitation program, with emphasis on strengthening the rotator cuff. If there is no improvement over 2 to 3 months, arthroscopy may be performed, which will reveal a partial tearing of the undersurface of the rotator cuff at or near its insertion into the humeral head. Arthroscopic débridement with a motorized shaver is performed to healthy, bleeding tissue.3,8 If the tear involves more than 50% thickness of the tendon insertion, repairing the tear is often recommended.14-16 Next, inspection of the subacromial space is performed. Frequently, there are no signs of impingement intraoperatively but, in chronic cases, secondary impingement may be present, with further tearing of the outer surface of the rotator cuff. In these cases, subacromial decompression with an acromioplasty should be performed (Fig. 7-1). Andrews and colleagues8 have reported on 34 athletes with partial tears who underwent arthroscopic débridement. Of these, 76% had excellent results and 9% had good results, and all were able to return to their previous athletic activities; 15% were rated as poor results and were not able to return to competitive throwing. Débridement of partial rotator cuff tears appears to reduce the pain in the athlete’s shoulder sufficiently to enable him or her to engage in a program of progressive strengthening exercises3 and to make a gradual return to competitive throwing, which usually takes 6 months or longer. Biceps-labral complex tears are believed to occur during the deceleration and follow-through phase of throwing. Large forces are placed on the proximal attachment of the biceps tendon at or near 90 degrees of abduction; the
The tensile lesions usually seen in the athlete’s shoulder occur as undersurface rotator cuff tears, biceps-labral complex tears, or both. The mechanism of injury in a primary tensile rotator cuff tear is deceleration of the rotator cuff as it resists horizontal adduction and internal rotation, anterior translation, and distraction forces seen during the deceleration phase of throwing. This results in eccentric tensile overload failure. Partial tears usually develop secondary to repetitive microtrauma.3 These are found in the region of the undersurface of the supraspinatus tendon and may extend posteriorly to the area of the infraspinatus tendon. These tears may also be found isolated to the infraspinatus tendon and posterior cuff capsule. It is not uncommon, especially in throwing athletes, for the athlete to experience pain only during the pitching motion. On physical examination, tenderness may be elicited over the supraspinatus or infraspinatus tendons, or both. If weakness is present; it is usually found by testing for external
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Figure 7-1. Acromioplasty—postarthroscopic subacromial decompression.
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humerus internally rotates at the same time as deceleration of elbow extension is occurring.17,18 There may also be some type of concurrent entrapment of the biceps-labral complex associated with glenohumeral laxity. Physical examination may reveal a popping or catching when the arm is in full abduction and external rotation, brought out by circumducting the humeral head on the glenoid—the clunk test. This test is performed with the patient in the supine position.18 The examiner’s hand lies posterior to the humeral head, applying an anterior directed force, while the opposite hand rests on the distal humerus, rotating the humerus. The patient’s arm is brought into the full overhead abducted position, assessing for a clunk or grind in the shoulder, suggesting a labral tear. At arthroscopy, a tear of the labrum in the anterosuperior quadrant at the insertion of the long head of the biceps is evident (Fig. 7-2). A partial tear of the biceps tendon near its origin may also be evident. Andrews and coworkers17 have suggested a mechanism for the anterosuperior glenoid labral tear. In 73 shoulder arthroscopies performed in pitchers and throwing athletes with labral tears, 83% had glenoid labral tearing at the biceps-labral complex anterosuperiorly; electrical stimulation of the biceps in 5 patients at arthroscopy produced tension in the biceps tendon and lifting up of the superior labrum off the glenoid. It was hypothesized that this eccentric contraction may cause tearing of the anterosuperior labrum.17 Treatment for this lesion usually entails limited arthroscopic débridement of the labral tear, if stable, as well as the biceps tendon if it is partially torn.3 If unstable, the labral tear should be repaired. Infrequently, the tear may propagate into the superior attachment of the middle and inferior glenohumeral ligaments, with the subsequent development of instability. If this is the case, the lesion should be repaired. Arthroscopic débridement is followed by rehabilitation.
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ROTATOR CUFF TEARS As noted, proposed mechanisms for rotator cuff tears in overhead throwing athletes have included eccentric tendon failure caused by overuse, secondary impingement from instability, and internal impingement of the rotator cuff on the posterior superior labrum.5,6,8,19-22 Most likely, these mechanisms all overlap somewhat and contribute to each individual’s rotator cuff injury to a different degree. In addition, a traumatic injury can result in an acute rotator cuff tear, although this is less common in the young athlete. Rotator cuff tears include a spectrum ranging from partialthickness to full-thickness tears, both of which can be managed arthroscopically with débridement or repair. It is generally agreed that any full-thickness tear should be repaired. Management of partial-thickness tears has been somewhat more controversial and continues to evolve. Results of rotator cuff débridement for partial tears have been favorable, but tears of more than 50% thickness are usually repaired.8,14-16,23,24 Arthroscopically, the depth of a tear is determined by estimating the distance of the intact cuff from the articular surface. That distance is then considered as a percentage of 14 mm, which is the size of the average supraspinatus footprint as determined by Dugas and colleagues.25 Again, the topic of rotator cuff tears in athletes will be discussed in more detail in later chapters.
GLENOHUMERAL LAXITY Generally, the diagnosis of shoulder laxity can be made on the basis of the history and physical findings. The athlete may have a history of documented anterior dislocation with subsequent redislocations, or the athlete may present only with the complaint of pain, clicking, or the so-called dead arm syndrome.26 In this syndrome, the athlete feels a sudden sharp or paralyzing pain when the shoulder is externally rotated forcibly in the abducted overhead position. The most reliable finding on physical examination is the apprehension test, in which the abducted arm is rotated externally while forward pressure is exerted on the humeral head. This pushes the humeral head forward against the anterior capsule. If the patient experiences pain and apprehension, this suggests anterior instability.
Figure 7-2. Biceps-labral complex tear.
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Approximately 50% of patients with shoulder subluxation are unaware of it.26 Therefore, physical examination, radiography, and arthroscopy become important aids in the diagnosis.27-29 After the patient is administered general anesthesia, the shoulder is examined and compared with the contralateral shoulder. Range of motion and anteriorposterior translation are assessed, and the clunk test is carried out. Next, diagnostic arthroscopy is performed to assess redundancy of the anterior capsule and glenohumeral ligaments.28,30 The glenoid labrum is evaluated and
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probed, looking for tears and detachment. A detachment of the inferior glenohumeral ligament–labral complex from the lower one half of the glenoid margin is most often associated with anterior instability.27-29 Under direct visualization using the arthroscope, the humeral head is pushed anteriorly, posteriorly, and inferiorly, and the amount of translation or subluxation is noted. This is helpful in deciding the main direction of instability, although it may be difficult to measure humeral head subluxation with arthroscopy. Also, the presence of a drive-through sign seen arthroscopically helps confirm the diagnosis of instability. The drive-through test is performed by sweeping the scope from superior to inferior between the glenoid and humeral head. If the scope can easily be driven through, the test is positive. If the labrum is torn, repair may be done arthroscopically or with an open procedure. A decision must be made regarding the treatment plan. Athletes with mild instability may be tried with strengthening exercises first29; if this fails, further intervention may be warranted. Athletes with moderate to severe instability may require an arthroscopic or open stabilization procedure. If there is an early true Bankart lesion, arthroscopic repair may be performed as described by Caspari,31 Johnson,32 and Morgan and Bodenstab.33 Postoperatively, the shoulder is immobilized in the adducted and internally rotated position in a shoulder immobilizer for 4 weeks to ensure soft tissue healing. At the American Academy of Orthopaedic Surgeons meeting in 1989, Caspari31 reported a 4% resubluxation rate for the arthroscopic Bankart repair, with 90% good or excellent results. Regardless of this early enthusiasm for the arthroscopic repair of the unstable shoulder, some surgeons still do not recommend this procedure for athletes returning back to contact sports.
such as in throwing, tennis, and swimming.35 It may also be caused by forceful entrapment associated with an avulsion sprain of the biceps-labrum complex between the humeral head and glenoid rim, such as a player diving to catch a baseball on the outstretched arm (Fig. 7-3). A significant percentage of labral tears in the throwing athlete involve the anterosuperior portion near the insertion of the long head of the biceps tendon and are not associated with instability.36 Pappas and associates37 have noted a functional instability from the torn hypermobile labrum. There was no increase in glenohumeral translation, but the patient felt insecure about the shoulder. It was theorized that there is clicking, catching, or locking in the joint secondary to the intermittent interposition of a partially attached fragment or bucket-handle tear between the glenoid and humeral head (Fig. 7-4). One must always be cautious because these functional tears may represent occult laxity and lead to overt instability. Arthroscopy is indicated for the athlete with persistent shoulder pain, symptoms of catching, and demonstrate a positive clunk test on physical examination.35 Andrews and Carson11 reported on arthroscopy in 73 athletes with labral tears and found 83% with anterosuperior tears. After arthroscopic débridement, 88% had good to excellent results at 13.5 months’ follow-up. Arthroscopic repair is indicated for unstable labral tears and will be discussed further in later chapters.
THROWER’S EXOSTOSIS The finding of a posterior glenoid exostosis in throwers with shoulder pain was first described in 1941 by Bennett, who studied a group of professional baseball players.3 The exostosis is located at approximately the 8-o’clock position on a right glenoid and is probably a secondary reaction associated
There is increasing experience regarding arthroscopic treatment of posterior instability. Treatment considerations are the same as those for anterior instability.34 Most athletes will respond to an aggressive exercise program, especially those with generalized ligamentous laxity. Arthroscopy should be considered for those who fail an adequate trial of conservative therapy. Again, a thorough examination under general anesthesia is mandatory. With current techniques, reverse Bankart lesions can be treated and repaired arthroscopically.
GLENOID LABRAL TEARS Not all labral tears are associated with instability.27 SLAP tears may occur with throwing and racquet sports or with some other type of deceleration injury. The mechanism of labral tearing can be caused by repetitive overhead activity,
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Figure 7-3. Anterior glenoid labral tear.
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needed before surgery is indicated. Diagnostic and operative arthroscopy has its role in the treatment armamentarium but caution must be exercised; treatment must be aggressive enough to return the athlete to competition in the shortest period of time but also conservative enough that it does not compromise the athlete’s subsequent performance. There are many factors to consider in the treatment process, thus making the definitive decision a difficult one. This chapter has briefly described the different lesions that may be encountered in the athlete’s shoulder and their arthroscopic management. These lesions are not mutually exclusive but may occur together or secondary to an underlying problem, which must be identified. The following chapter in this section discuss these pathologies in detail and explain different treatment options. Figure 7-4. Anterior glenoid labral tear.
References
with repeated microtrauma and tearing of the posterior and inferior capsule off its glenoid insertion.3 For many years, it was believed that the exostosis was calcification in the long head of the triceps tendon insertion. Arthroscopic resection of this lesion with posterior capsular release has been performed on many pitchers and relieved their symptoms, allowing them to return to competitive pitching.
ACROMIOCLAVICULAR JOINT INJURIES Athletes who lift weights as part of their training program and weightlifters are prone to acromioclavicular joint injuries. These include osteolysis of the distal clavicle secondary to longitudinal shear or compressive forces across the joint and partial or complete acromioclavicular separations secondary to post-traumatic injury to the joint. The athlete usually complains of a dull ache or pain over the acromioclavicular joint. Conservative treatment is tried first, consisting of an NSAID, physical therapy, modification of physical activity and, finally, steroid injection into the joint. If this fails, arthroscopic débridement of the acromioclavicular joint may be performed, with decompression on the acromion and clavicular side of the joint.
CONCLUSIONS AND SUMMARY The athlete with shoulder pathology should be treated conservatively and aggressively at the same time. Usually, the diagnosis is established with the history and physical examination. Ancillary tests are important and may be needed to confirm or substantiate the clinical impressions. Depending on the pathology and time constraints of the athlete, most are first placed on a rehabilitation program. Three months of conservative treatment are generally
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1. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:216, 1986. 2. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 3. Andrews JR, Angelo RL: Shoulder arthroscopy for the throwing athlete. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 79. 4. Jobe FW, Glousman RE: Rotator cuff dysfunction and associated glenohumeral instability in the throwing athlete. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 85. 5. Walch G, Boileau J, Noel E, Donnell ST: Impingement of the deep surface of the supraspinatus tendon on the posterior superior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1:238, 1992. 6. Jobe CM: Posterior superior glenoid impingement: expanded spectrum. Arthroscopy 11:530, 1995. 7. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology, Part 1: Pathoanatomy and biomechanics. Arthroscopy 19:404, 2003. 8. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117, 1985. 9. Meister K, Andrews JR: Classification and treatment of rotator cuff injuries in the overhead athlete. J Orthop Sports Phys Ther 18:413, 1993. 10. Paley KJ, Jobe FW, Pink MM, et al: Arthroscopic findings in the overhead throwing athlete: Evidence for posterior internal impingement of the rotator cuff. Arthroscopy 16:35, 2000. 11. Andrews JR, Carson WG: The arthroscopic treatment of glenoid labrum tears in the throwing athlete. Orthop Trans 8:44, 1984. 12. Gross ML, Brenner SL, Esformes I, Sonzogni JJ: Anterior shoulder instability in weight lifters. Am J Sports Med 21:599, 1993. 13. Davidson RA, El Attrache NW, Jobe CM, Jobe FW: Rotator cuff and posterior-superior glenoid labrum injury associated
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14.
15. 16.
17.
18.
19.
20.
21.
22. 23. 24.
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with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 4:384, 1995. Conway JE: Arthroscopic repair of partial-thickness rotator cuff tears and SLAP lesions in professional baseball players. Orthop Clin North Am 32:443, 2001. Gartsman GM, Milne JC: Articular surface partial-thickness rotator cuff tears. J Shoulder Elbow Surg 4:409, 1995. Millstein ES, Snyder SJ: Arthroscopic management of partial, full-thickness, and complex rotator cuff tears: Indications, techniques, and complications. Arthroscopy 19:189, 2003. Andrews JR, Carson WG, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. Andrews JR, Carson WG, Ortega K: Arthroscopy of the shoulder: Technique and normal anatomy. Am J Sports Med 12:1, 1984. Nirschl RP. Shoulder tendonitis. In Pettrone FA (ed): Symposium on Upper Extremity Injuries in Athletes (American Academy of Orthopaedic Surgeons). St. Louis, Mosby, 1986, pp 322-337. Jobe FK, Kvitne RS: Shoulder pain in the overhead or throwing athlete: The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963, 1989. Jobe FK, Pink MM: Classification and treatment of shoulder dysfunction in the overhead athlete. J Orthop Sports Phys Ther 18:427, 1993. Jobe CM: Superior glenoid impingement: Current concepts. Clin Orthop 330:98, 1996. Altchek DW, Carson EW: Arthroscopic acromioplasty: Current status. Orthop Clin North Am 28:157, 1997. Snyder SJ, Pachelli AF, Del Pizzo W, et al: Partial thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1, 1991.
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25. Dugas JR, Cambell DA, Warren RF, et al: Anatomy and dimensions of rotator cuff insertions. J Shoulder Elbow Surg 11:498, 2002. 26. Zarins B, Rowe CR: Current concepts in the diagnosis and treatment of shoulder instability in athletes. Med Sci Sports Exerc 16:444, 1984. 27. Ellman H: Shoulder arthroscopy: Current indications and techniques. Orthopedics 11:45, 1988. 28. McGlynn FJ, Caspari RB: Arthroscopic Findings in the Subluxating Shoulder. Rockville, Md, Aspen, 1991. 29. O’Brien SJ, Warren RF, Schwartz E: Anterior shoulder instability. Orthop Clin North Am 18:395, 1987. 30. Yahiro MA, Matthews LS: Arthroscopic stabilization procedures for recurrent anterior shoulder instability. Orthop Rev 18:1161, 1989. 31. Caspari RB: Arthroscopic reconstruction for anterior shoulder instability. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 57. 32. Johnson LL: Shoulder arthroscopy. In Johnson LL (ed): Arthroscopic Surgery, Principles and Practice. St. Louis, Mosby, 1986. 33. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111, 1987. 34. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409, 1987. 35. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901, 1991. 36. Andrews JR, Gidumal RH: Shoulder arthroscopy in the throwing athlete: Perspectives and prognosis. Arthroscopy 6:565, 1987. 37. Pappas AM, Goss TP, Kleinman PK: Symptomatic shoulder instability due to lesions of the glenoid labrum. Am J Sports Med 11:279, 1983.
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CHAPTER 8 Arthroscopic Techniques
of the Shoulder William B. Geissler, Richard B. Caspari, and Scott B. Reynolds
shoulder.2 The patient is further stabilized with tape running from the side rails across the pelvis. After the anesthesiologist has checked the position of the head, it is covered and lightly taped to prevent any displacement during the procedure (Fig. 8-1). A skin traction device is applied to the forearm after the patient has been prepared and draped, and the arm is suspended by an overhead rope and pulley traction apparatus. The arm is placed in approximately 30 to 40 degrees of abduction and 20 degrees of forward flexion. The arm is suspended by 10, 15 or, rarely, 20 pounds of traction, which provides distraction and inferior subluxation of the humerus. This displacement allows the surgeon to see and work in the anteroinferior area of the glenoid, where most pathology related to anterior instability is located. In the beach chair position, the patient is placed as if sitting in a chair.3 The head must be carefully supported in a neutral position to prevent hyperextension. The body is again supported and stabilized in place. The operative arm is draped free to allow full access to the shoulder. Temporary traction may be applied by a surgical assistant, if required, during the procedure.
The techniques of diagnostic and surgical shoulder arthroscopy have become a valuable adjunct in the management of shoulder disorders. A thorough understanding of the anatomy of the shoulder girdle is mandatory as the complexity of arthroscopic shoulder procedures continues to expand. Precise placement of arthroscopic portals is imperative in the shoulder because of the proximity of many neurovascular structures and the muscles that are perforated. This chapter reviews the operative technique and anatomy pertaining to establishing the various portals for arthroscopic surgery of the shoulder.
OPERATIVE TECHNIQUE The importance of the operating room setup cannot be overemphasized for a successful and efficient arthroscopic shoulder procedure. The procedure may be performed under general endotracheal anesthesia or interscalene block. Most surgeons prefer general endotracheal anesthesia, particularly if the lateral decubitus position is used. Intubation in this position is difficult if the patient becomes uncomfortable and may require re-preparing and draping. Interscalene blocks are more frequently used when the patient is placed in the beach chair position. This allows the patient to help position himself or herself for the procedure, and the anesthesiologist has more optimal access to the patient’s airway if the need should arise.
In both positions, the monitor, light, and power equipment source are placed opposite the patient’s shoulder in front of the surgeon. The scrub nurse and Mayo stand can be situated just in front of the surgeon toward the foot of the table for both positions, or at the head of the operating table for the lateral decubitus position (Fig. 8-2). Using these setups, the surgeon has easy access to the whole shoulder without having to move any equipment or personnel.4 The scrub nurse is in the ideal position to pass instruments and to assist the surgeon when needed. The standard-sized instruments that are used for the knee may be used for the shoulder.
Vital information is gained from examination of the shoulder under anesthesia, and this opportunity should not be missed. The shoulder girdle muscles are relaxed, allowing the examiner to translocate the humeral head on the glenoid freely and measure any existing instability. The evaluation also should include range of motion of both shoulders, noting any limitations in passive motion suggestive of adhesive capsulitis. Occasionally, increased external rotation in abduction is observed, reflecting anterior capsular laxity and possible anterior instability. In cases of shoulder subluxation, the information obtained from the clinical examination is correlated with the arthroscopic findings to confirm the diagnosis.1 After the clinical examination, the patient is placed in the lateral decubitus or beach chair position, depending on the surgeon’s preference. In the lateral decubitus position, the patient is placed on his or her side with the affected shoulder up. The patient is supported by an inflatable beanbag or kidney rests, or both. It is important to tilt the patient back 30 degrees to allow easier access to the front of the
EXTERNAL ANATOMY Knowledge of the external anatomy and palpable landmarks of the shoulder is essential for precise portal placement. Palpable bony landmarks include the clavicle and coracoid anteriorly, the acromion laterally, and the scapular spine posteriorly. The coracoid is located just inferior to the palpable acromioclavicular joint. It is important to note the location of the coracoid when making an anterior portal because the neurovascular bundle runs medial to it. The posterior lateral corner of the acromion is almost always palpable, no matter how large or obese the patient. This is 105
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Figure 8-1. Patient positioning. The patient is placed in the lateral decubitus position and slanted back 30 degrees for easier access to the front of the shoulder. Figure 8-3. External anatomy and relative positions of arthroscopic portals. The letter “X” anteriorly marks the coracoid process. Note the position of the posterior portal medial to the posterolateral edge of the acromion.
It is important to maintain a portal in the shoulder once it has been established, because the chance of reintroducing an instrument or cannula exactly through the same hole in the tissue is remote.5 Attempts to re-establish a previous portal not only lead to unnecessary soft tissue damage but also promote extravasation of irrigation fluid into the soft tissues, obliterating bony landmarks. Therefore, interchangeable cannula systems are used that allow passage of the arthroscope and motorized instruments through the same cannula.
Figure 8-2. Lateral decubitus position. The arm is suspended 30 to 40 degrees. Note the Mayo stand at the head of the table. The light source and camera cords are passed under the arm and the shaver above.
an important landmark, because the placement of the initial posterior portal is based on its location. The shoulder is surrounded by a thick, soft tissue envelope that can make palpation of landmarks difficult, particularly in obese or well-muscled individuals. It is often helpful to draw the bony landmarks on the shoulder skin to help maintain proper orientation. These should be palpated and drawn before the introduction of irrigation fluid, which may extravasate and further obliterate identification of these landmarks (Fig. 8-3).
PORTALS AND ANATOMY Establishing a portal in the shoulder involves perforation of several layers of tissue. Also, in some patients, the shoulder joint lies a considerable distance from the skin.
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Langer’s lines are observed during skin incisions for portal placement. The anterior and posterior portal skin incisions are vertical, aiming at the axillary fold. The lateral portal incision is horizontal, and the superior portal incision is established in the anteroposterior direction. When making an incision for a portal, only the skin is cut, avoiding deep plunges with the knife.
Posterior Portal The posterior portal is the most frequently used portal for shoulder arthroscopy. It allows almost complete visualization of the entire glenohumeral joint. Precise positioning of the posterior portal is important, because improper placement can make viewing of the joint difficult and will displace the normal position of the anterior portal if the inside-out technique is used. The posterior portal is located approximately 2 cm distal and 1 cm medial to the posterolateral corner of the acromion. This portion of the acromion is almost always palpable, regardless of the size of the patient. It is important to avoid the tendency to stray laterally down the arm and to remain 1 cm medial to the edge of the acromion when
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ARTHROSCOPIC TECHNIQUES OF THE SHOULDER
making this portal. The portal is located in the usually palpable soft spot of the shoulder. The glenohumeral joint may be insufflated with irrigation solution before insertion of the cannula, depending on the surgeon’s preference. After the skin is incised, a sharp cannula is inserted and directed toward the coracoid on the opposite side of the shoulder. The cannula passes through the deltoid muscle and a portion of the subdeltoid bursa. It then perforates the muscular belly of the infraspinatus or passes between the interval of this muscle and the teres minor. The cannula finally pierces the capsule and synovium to enter the joint. The posterior portal is relatively safe when placed in the correct position. The axillary nerve passes below the teres minor through the quadrilateral space to innervate it and the deltoid. The nerve becomes at risk if the cannula is advanced too far inferiorly, passing below rather than above the teres minor. The suprascapular nerve passes around the scapular spine after it has innervated the supraspinatus to supply the infraspinatus muscle. The nerve passes 2 cm medial to the posterior edge of the glenoid. It becomes at risk if the cannula is advanced too far medially along the glenoid neck.
Anterior Portal The anterior portal is used mainly to pass instrumentation into the joint. The anterior glenoid neck and labrum, articular surface of the rotator cuff, and intra-articular portion of the biceps tendon are easily accessible through this portal. The arthroscope may be placed through the anterior portal to evaluate pathology of the glenohumeral joint further if not properly seen from the posterior portal. This is particularly helpful when judging the effectiveness of the anterior inferior glenohumeral ligament from a different perspective in patients with a history of shoulder subluxation, as well as when viewing posterior shoulder pathology. The anterior portal may be made in one of two ways. One method is to pass the arthroscope from the posterior portal across the joint to the desired location on the anterior capsule. The desired location on the capsule lies within a triangle bounded by three easily identifiable landmarks. The triangle is formed by the biceps tendon superiorly, the intra-articular portion of the subscapularis inferiorly, and the anterior glenoid medially. The arthroscope is advanced against the anterior capsule and withdrawn from its sheath. A sharp obturator is placed in the sheath, and this is passed through the capsule to tent the skin anteriorly. A small skin incision is made, and a cannula is placed over the obturator as it exits the skin. Most cannulas are slightly larger than the arthroscopic sheath and slide snugly over it. The cannula then follows the obturator as it is withdrawn posteriorly to enter the joint. The obturator is removed, and the arthroscope is replaced back into its sheath. Using this method, the cannula passes through the rotator cuff interval between the subscapularis inferiorly and the
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supraspinatus superiorly. It then pierces the anterior deltoid to exit the skin. Once this portal has been established, it should never be lost because of the risk of extravasation of fluid into the soft tissues. The anterior portal may also be established directly by passing a spinal needle from the anterior shoulder into the joint. If the position of the needle is satisfactory intra-articularly, a cannula is passed through a small skin incision, reproducing the tract of the needle into the joint. This method is more difficult because of the thick, soft tissue envelope of the shoulder, and following the exact path of the spinal needle with a cannula is not easy. Occasionally, this method is required when the arthroscope sheath cannot be advanced across the joint secondary to improper placement of the original posterior portal or severe adhesive capsulitis. The anterior portal is relatively safe if properly placed and close attention is paid to the palpable external landmarks. Whether the inside-out or direct method of portal placement is used, the position of the portal must always be lateral to the palpable coracoid. The conjoined tendon inserts on the coracoid. The musculocutaneous nerve runs along the medial border of the conjoined tendon approximately 3 to 7 cm inferior to the coracoid. Any portal placed medial to the coracoid places this nerve at unnecessary risk. The anterior portal should also not be placed below the subscapularis tendon. The axillary nerve passes below the subscapularis to innervate the deltoid and will be at jeopardy if the portal is placed too inferiorly.
Subacromial Portals A thorough arthroscopic examination of the shoulder includes the glenohumeral joint and subacromial space. Subacromial portals are useful to examine the superior surface of the rotator cuff for full- or partial-thickness tears and the undersurface of the acromion for signs of impingement. Arthroscopic subacromial decompression, distal clavicle resection, and débridement or repair of the rotator cuff are procedures that can usually be performed through these portals. A considerable amount of irrigation fluid may be extravasated into the soft tissues after arthroscopy of the subacromial space. Thus, the subacromial space is usually approached after examination of the glenohumeral joint. The arthroscope sheath with a sharp obturator is placed through the original skin incision for the posterior glenohumeral portal and tracked subcutaneously toward the posterior edge of the acromion. It is then advanced under the acromion into the subacromial space, aiming for the anterolateral corner of the acromion. The undersurface of the acromion should be palpated with the arthroscope sheath to confirm its position in the subacromial space. The sharp obturator is replaced with the arthroscope and inflow is provided through the scope sheath with an infusion
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pump or through a separate anterior portal. Typically, an irrigation pump is used to supply inflow through the arthroscope sheath. If not, a second portal for inflow is usually required because bleeding into the subacromial space can be profuse and a high flow rate may be required. To establish the anterior inflow portal, the arthroscope sheath and obturator are advanced past the anterior acromion and out the previous skin incision for the anterior glenohumeral portal. A cannula is placed over the arthroscope sheath and guided into the subacromial space as the sheath is retracted. This portal can also be used as a working portal for distal clavicle excision or for suture management during a rotator cuff repair. An additional working portal is frequently made laterally to the acromion to pass instrumentation or the arthroscope. The position of this portal is approximately 3 cm distal to the anterolateral corner of the acromion (Fig. 8-4). An incision is made just through the skin to avoid any possible injury to the underlying deltoid muscle or the axillary nerve. A blunt obturator is passed obliquely and can be seen to enter the subacromial space with the arthroscope. The position of this portal places the instrumentation parallel to the anterior acromion and in an ideal position to resect the coracoacromial ligament, if required. The position of the axillary nerve should always be kept in mind when making this portal because it runs 5 cm distally to the lateral edge of the acromion under the deltoid to supply this muscle.
Additional Portals Although the portals previously described are the most commonly used during shoulder arthroscopy, additional portals can be used. Accessory portals for anchor placement and suture passage are necessary for various labral repairs. These portals include the 5 o’clock portal, anterosuperolateral portal, Port of Wilmington portal, posterolateral portal,6 and Nevaiser’s portal.7 The 5 o’clock portal, established about 1 cm inferiorly and 2 to 3 cm laterally to the anterior
portal through the most lateral portion of the subscapularis tendon, is helpful for the placement of anchors along the anteroinferior glenoid during a Bankart repair. The anterosuperolateral portal is located approximately 1 to 2 cm laterally to the anterolateral corner of the acromion. The Port of Wilmington portal is established approximately 1 cm anteriorly and 1 cm laterally to the posterolateral corner of the acromion. These two portals are essential for anchor placement during repair of SLAP lesions. The anterosuperolateral portal is also useful for placing medial row anchors during double-row rotator cuff repairs. The posterolateral portal is placed about 1 cm inferiorly and 2 to 3 cm laterally to the posterior portal, entering through the lateral portion of the posterior cuff. This allows access to the posteroinferior glenoid for anchor placement during repair of posterior Bankart lesions. Finally, Nevaiser’s portal is located just posteriorly and medially to the acromioclavicular joint, through the palpable soft spot in this area. This portal can be useful for rotator cuff repairs, as well as for passage of sutures during SLAP repairs. All these portal locations are established with an outside-in technique after localizing with a spinal needle. The exact angle and location are adjusted based on the placement of the spinal needle.
SUMMARY A knowledge of shoulder arthroscopy is imperative as it continues to evolve and become popular for the diagnosis and management of shoulder disorders. Arthroscopy of the shoulder has helped advance the understanding of various shoulder maladies, such as the complex relationship between impingement and instability in the throwing athlete. As with any surgical technique, a thorough knowledge of the anatomy of the shoulder girdle relative to portal placement is essential before undertaking this successful procedure.
References
Figure 8-4. Ideal position of lateral subacromial portal. This is initially determined with a spinal needle. The position of the needle in the subacromial space is viewed arthroscopically and modified accordingly.
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1. McGlynn FJ, Caspari RB: Arthroscopic findings in the subluxating shoulder. Clin Orthop Relat Res 183:173-178, 1984. 2. Caspari RB: Shoulder arthroscopy: A review of the present state of the art. Contemp Orthop 4:523, 1982. 3. Skyhar MJ, Altchek DW, Warren RF et al: Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy 4:256-259, 1988. 4. Caspari RB: Instrumentation and operating room organization for arthroscopy of the shoulder. In McGinty JB (ed): Arthroscopic Surgery Update, Techniques in Orthopaedics. Rockville, Md, Aspen, 1985, p 155. 5. Andrews JR, Carson WG: Shoulder joint arthroscopy. Orthopedics 6:1157, 1983. 6. Lo IK, Lind CC, Burkhart SS: Glenohumeral arthroscopy portals established using an outside-in technique: Neurovascular anatomy at risk. Arthroscopy 20:596-602, 2004. 7. Nord KD, Masterson JP, Mauck BM: Superior labrum anterior posterior (SLAP) repair using the Neviaser portal. Arthroscopy 20(Suppl 2):129-133, 2004.
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CHAPTER 9 Tensile Failure of the Rotator Cuff Christopher W. Baker and Brian D. Busconi
Rotator cuff injury in the athlete can have several different causes. Factors related to the development of rotator cuff tears can be classified as intrinsic (changes to cuff vasculature or the normal aging process), extrinsic (impingement caused by abnormalities in the subacromial arch), or traumatic (excessive tensile load to the rotator cuff caused by a single traumatic event or repetitive microtrauma).1 This latter mechanism, which can lead to the injury complex known as primary tensile failure of the rotator cuff,1,2 is most typically seen in the throwing or overhead athlete participating in sports such as baseball, tennis, volleyball, and team handball. It is a complex problem that can create a significant clinical challenge.1,3
pitching motion have divided it into six phases, separated by reproducible points within the motion. These phases include the wind-up, early cocking (stride), late cocking, acceleration, deceleration, and follow-through.9 It is during this throwing motion that the shoulder and tissues surrounding it are subjected to extreme stress, position, and force.3,7,8 The late cocking, acceleration, and deceleration phases generate the largest forces and account for most injuries.5,9 The shoulder is maintained in about 90 to 110 degrees of abduction throughout the throw, but ranges from 30 degrees of abduction at maximal cocking to 10 degrees of adduction at follow-through. External rotation is maximized at around 175 degrees during the late cocking phase and moves to around 105 degrees of internal rotation during the throw. This can generate arm angular velocities in excess of 7000 to 8000 deg/sec and rotational torques more than 70 N•m, with shear forces ranging from 300 to 400 N and compressive forces more than 1000 N.6,11 During deceleration, forces can approach ⫺500,000 deg/sec2. The extreme range of external rotation, coupled with the tremendously high joint forces, can exceed the physiologic limits of the joint, leading to failure.
The repetitive throwing motion is a dynamic activity that places extraordinary stresses on the athlete’s shoulder, capsuloligamentous complex and, in particular, rotator cuff.1,3-7,9 Remarkably high forces are generated by the cuff musculature, specifically during the deceleration phase of throwing, to slow the rapidly moving shoulder. These forces, applied repetitively with the throwing motion, are believed to be primary factors underlying the mechanism for tensile rotator cuff failure.
FORCES AND MUSCLE ACTIVITY
Electromyography data collected throughout the phases of the throwing motion have allowed for the evaluation of muscular firing patterns.5,8,9 During the wind-up phase, muscle activity is low, below 21% of maximal voluntary contraction. Small forces are placed on the shoulder and few injuries occur during wind-up. During the early cocking phase, muscle activity increases. The serratus anterior and trapezius muscles demonstrate moderate to high activity and, in concert with the middle deltoid and supraspinatus, help keep the humeral head congruent with the glenoid. The late cocking and acceleration phases are when the shoulder begins to experience an increase in forces. It is also when the shoulder is maximally externally rotated and horizontally abducted.3 The subscapularis, pectoralis major, and latissimus dorsi all demonstrate high to very high activity and provide stability to the joint. The action of the deltoid begins to diminish ,and the rotator cuff muscles increase their activity. The infraspinatus and teres minor show very high activity, whereas the supraspinatus is the least active. The rotator cuff muscles provide a compressive force, contributing to the stability of the joint. During deceleration and follow-through, the excess kinetic energy not transferred to the ball is dissipated
The shoulder is the most mobile joint in the body. It is designed to provide stability, which allows a wide range of motion in multiple directions. Motion is determined by glenohumeral configuration, soft tissue flexibility, and a balance between dynamic (muscle) and static (ligament, tendon) shoulder stabilizers.1,10 This leads to a delicate equilibrium of stability and mobility, especially in the overhead athlete who is trying to generate a tremendous amount of energy.4 The athlete must maximally accelerate and decelerate the arm over a short period of time while maintaining precise control over the object being thrown.9 This places extreme demands on the shoulder. The baseball pitch is the biomechanical model most used for many overhead throwing motions.3 This motion is a kinetic chain activity in which energy derived from the lower extremity is transferred through the pelvis and trunk rotationally, with subsequent release through the upper extremity. As a segment of the body undergoes acceleration, the succeeding segment is left behind.5 High-speed cinematography and three-dimensional analysis of the 111
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through the shoulder. This is characterized by a powerful deceleration force provided by the posterior musculature. Opposing muscles tend to fire simultaneously to accomplish this control. The teres minor demonstrates the highest activity of the posterior musculature, and the middle and posterior heads of the deltoid are the most active antagonists. The subscapularis also demonstrates high activity as well in maintaining humeral head position and preventing subluxation. Injury to the rotator cuff can occur during the deceleration phase as it resists horizontal adduction, internal rotation, anterior translation, and distraction forces. This repetitive action may result in microtrauma over time and lead to tensile failure of the rotator cuff.7
PATHOGENESIS OF TENSILE FAILURE With repeated injury, articular-sided partial-thickness tears and intratendinous tears can develop in the rotator cuff.7,12 This has been referred to as primary tensile failure of the rotator cuff.2 As noted, the rotator cuff is exposed to tremendous forces during the deceleration phase. The rotator cuff must not only offset these high-energy forces but also stabilize the humeral head within the glenoid. These eccentric tensile forces can overload the rotator cuff tendons, resulting in microtraumatic injuries, which accumulate with repetitive throwing.8 This is typically believed to occur during the deceleration phase as the rotator cuff musculature resists horizontal adduction, internal rotation, anterior translation, and distraction forces.1 It usually involves the undersurface of the posterior half of the supraspinatus and superior half of the infraspinatus. Once believed to be caused exclusively by repetitive microtrauma, it is now believed to be multifactorial in origin. Intrinsic factors, such as age-related changes in vascularity of the cuff or other metabolic alterations, may play a role in the development of partial-thickness articular-sided tears.1 Similarly, the structure of the tendon itself may also be a contributing factor. The rotator cuff tendon is composed of five layers, which predisposes it to the development of internal shear forces.12 The bursal side is more resistant to rupture and elongates with a tensile load, whereas the articular side does not stretch and tears easily. Cadaveric studies have shown that partial-thickness articular-sided tears will develop at only 15 degrees of shoulder abduction, and that tendon failure can occur at 90 degrees and more of abduction. Propagation of the tear from the articular side to the bursal side may also occur at increasing degrees of abduction, such as in overhead athletes who undergo repetitive strains at extremes of motions. Extrinsic factors may also be involved in the development of partial-thickness, articular-sided, rotator cuff pathology in the overhead athlete. Subacromial impingement, as a result of narrowing of the supraspinatus outlet by anatomic variations in the coracoacromial arch, may cause
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partial tears by irritation of the cuff. Although originally believed to be primarily a source of bursa-sided tears, finite element models have demonstrated that external impingement can result in high enough stress to cause not only bursa-sided tears, but intratendinous and articularsided tears as well.1,12 Similarly, subacromial impingement may play a role in aggravating many partial-thickness tears. However, bursa-sided tears are still more commonly associated with subacromial impingement. Internal impingement may also be a contributing factor in the development of articular-sided rotator cuff tears. Internal impingement is abnormal contact between the posterosuperior aspect of the glenoid and the undersurface of the rotator cuff.5,12 This can be the result of many factors, including anterior instability, posterior capsular tightness, decreased humeral retroversion, tension overload, poor throwing mechanics, and scapular muscle imbalance. Repetitive throwing may cause progressive injury or attenuation of the static stabilizers of the shoulder joint, leading to increased glenohumeral translation.1 Consequently, increased rotator cuff activity is required to counteract this increased humeral translation or subluxation.7 Over time, these dynamic stabilizers may fatigue, allowing the rotator cuff to impinge on the coracoacromial arch, with resultant rotator cuff injury. However, many overhead athletes will have adaptive ligamentous laxity of the shoulder to begin with.12 Therefore, it is important to be able to differentiate which components of the clinical picture are adaptive and which are pathologic in development. As noted, the pathogenesis of articular-sided, partialthickness, rotator cuff tears is likely multifactorial. Interactions between trauma, intrinsic, and extrinsic factors may all contribute to the development of primary tensile failure of the rotator cuff.1,5,7,8,12
DIAGNOSIS The vast majority of athletes with partial-thickness rotator cuff tears will present with a chief complaint of shoulder pain and diagnosis may be extremely challenging, because many conditions manifest with this finding.1,3,9,12 A careful and complete history that details the precise occurrence and precipitation of symptoms is necessary. The pain of a rotator cuff tear is classically described as persisting, even at rest, or as night pain. The location of pain may help delineate the causative factor. Anterior pain may be associated with subscapularis, biceps tendon, or capsulolabral injury, anterolateral pain is commonly seen with supraspinatus injury, and posterior pain can be seen with infraspinatus or capsulolabral injury.5,8 Instability symptoms may include a feeling of the arm going dead or a sensation of subluxation. The examiner should determine which phase of the throwing motion reproduces symptoms. Patients with anterior instability will experience pain, dead arm, or
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subluxation symptoms during the late cocking or early acceleration phase. Posterior subluxation typically manifests with pain during the follow-through phase. Pain related to certain precipitating activities might suggest a diagnosis of tendonitis or impingement. However, these distinctions are not always clear, making diagnosis difficult. A thorough physical examination is crucial and should attempt to isolate the structures that are responsible for the symptoms. The cervical spine, including range of motion, tenderness, and Spurling’s maneuver, should always be assessed to ensure that the pain is not radicular in nature.12 Inspection for asymmetry and atrophy are initial steps. Atrophy, especially of the infraspinatus fossa, may indicate chronic rotator cuff dysfunction or suprascapular nerve injury.9 Scapular dyskinesis may be a primary or secondary problem, and may be caused by fatigue or intra-articular glenohumeral pathology.3 Documentation of active and passive range of motion and muscle strength should also be preformed. Increased external rotation of the dominant shoulder compared with the nondominant arm may be a normal manifestation. Some throwers will also demonstrate a normal loss of internal rotation, which is also a common finding in an injured pitcher. Tenderness over the supraspinatus insertion or over the subacromial bursa would direct attention to impingement of the rotator cuff. Marked improvement in symptoms with local anesthetic infiltration of the bursa would support the subacromial space as the primary area of pathology. Loss of supraspinatus muscle strength, with resolution of pain after subacromial injection, suggests the presence of a full-thickness rotator cuff tear, whereas maintenance of strength after injection suggests inflammation or an articular surface or intratendinous tear. Ligamentous stability is tested in the anterior, posterior, and inferior directions and is mandatory in the young athlete because of the possibility of a coexistent internal impingement.12 These tests are performed on both shoulders and the results compared. The sulcus sign, Jobe’s test, and apprehension and relocation tests may all be performed, but may be difficult to interpret by inexperienced clinicians.3,9 The O’Brien test may help distinguish biceps tendon lesions, and impingement tests may delineate acromioclavicular pathology. A thorough neurovascular examination should also be performed distally in all cases. Radiographic studies complete the evaluation, even though they are frequently unrevealing. Os acromiale, subacromial spurs, and markedly curved or hook-shaped acromions may play a role in extrinsic rotator cuff impingement and can be detected with x-ray.5,8,12 Similarly, the anteroposterior view (x-ray) should be assessed for bony Bankart or Hill-Sachs lesions.9 Historically, arthrography and bursography have been used to aid in the diagnosis of partialthickness tears, but their accuracy has come under scrutiny. As a result, ultrasound and magnetic resonance imaging
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(MRI) are being used more often. Ultrasound has been reported to have a high sensitivity and specificity for the diagnosis of partial-thickness tears, but is extremely user dependent, making it less available. MRI, with multiple techniques available, demonstrates similar accuracy rates as ultrasound when diagnosing partial-thickness tears, and has the added benefit of being able to diagnose concomitant pathologic lesions. Despite a thorough examination and appropriate imaging, diagnostic arthroscopy may still be needed to diagnose a partial-thickness rotator cuff tear accurately.
TREATMENT OPTIONS For the throwing athlete suspected of having an isolated, partial-thickness, rotator cuff tear, the initial approach to management is nonoperative.5,8,9,12 This includes modification of activities, such as avoidance of overhead painprovoking maneuvers, and a short course of nonsteroidal anti-inflammatory drugs (NSAIDs).This is followed by a dedicated physical therapy program, with attention directed toward maintaining or regaining normal shoulder kinematics. This includes stretching, use of cryotherapy, and gradual range-of-motion (ROM) and strengthening exercises addressing the rotator cuff and scapular stabilizers. Corticosteroid injections can also be used, but multiple injections should be approached with caution because they could damage the rotator cuff tendon and should be completely avoided in the young athlete.1 For those athletes with concurrent shoulder instability or internal impingement, a similar initial course consisting of activity modification, NSAIDs, and physical therapy is used. Despite conservative measures, spontaneous healing of partial-thickness tears is unlikely and most progress to full-thickness tears. The absolute indications for surgical treatment of partialthickness rotator cuff tears continue to evolve.1,12 Operative treatment is typically reserved for patients with persistent symptoms who have failed conservative management, usually after 3 to 6 months.5,8 Additional factors are also considered, including the type and extent of the tear, occupation and activity level of the patient, and presence of additional intra-articular pathology. The timing can vary and multiple surgical options are available, ranging from simple débridement to repair.
SUMMARY Extraordinary stresses are placed on the athlete’s shoulder during the throwing motion. The rotator cuff serves to help maintain the glenohumeral relationship during the early phase of throwing, and decelerate the arm during the latter stages. A number of structures are subjected to these extreme forces, especially during the deceleration phase of the throwing motion. It is during this phase that the rotator
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cuff is most vulnerable to injury. Tensile failure of the rotator cuff (partial-thickness articular-sided tears) typically occurs during this phase. Initially believed to be traumatic in nature, it is now believed that there are a number of causative factors. Diagnosis can be difficult, and a thorough physical examination supplemented with radiographic imaging are necessary. Nonoperative treatment remains central to the management of these injuries.
References 1. Fukuda H: The management of partial-thickness tears of the rotator cuff. J Bone Joint Surg Br 85:3-11, 2003. 2. Andrews JR: The athlete’s shoulder: biomechanics, diagnosis and treatment. Presented at the American College of Sports Medicine Annual Meeting (Joseph B. Wolffe Memorial Lecture). Salt Lake City, Utah, May 22, 1990. 3. Limposvati O, Elattrache NS, Jobe FW: Understanding shoulder and elbow injuries in baseball. J Am Acad Orthop Surg 15:139-147, 2007. 4. Van Der Hoeven H, Kibler WB: Shoulder injuries in tennis players. Br J Sports Med 40:435-440, 2006.
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5. Park SS, Loebenberg ML, Rokito AS, Zuckerman JD: The shoulder in baseball pitching: biomechanics and related injuries—part 1. Bull Hosp Jt Dis 61:68-79, 2002-2003. 6. Borsa PA, Dover GC, Wilk KE, Reinold MM: Glenohumeral range of motion and stiffness in professional baseball pitchers. Med Sci Sports Exerc 38:21-26, 2006. 7. Mazoue CG, Andrews JR: Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med 34:182-189, 2006. 8. Park SS, Loebenberg ML, Rokito AS, Zuckerman JD: The shoulder in baseball pitching: biomechanics and related injuries—part 2. Bull Hosp Jt Dis 61:80-88, 2002-2003. 9. Altchek DW, Dines DM: Shoulder injuries in the throwing athlete. J Am Acad Orthop Surg 3:159-165, 1995. 10. Baltaci G, Tunay VB: Isokinetic performances at diagonal pattern and shoulder mobility in elite overhead athletes. Scand J Med Sci Sports 14:231-238, 2004. 11. Sabick MB, Torry MR, Kim YK, Hawkins RJ: Humeral torque in professional baseball pitchers. Am J Sports Med 32: 892-898, 2004. 12. Matava MJ, Purcell DB, Rudzki JR: Partial-thickness rotator cuff tear. Am J Sports Med 33:1405-1417, 2005.
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CHAPTER 10 Subacromial Impingement Sara L. Edwards, John-Erik Bell, and Louis U. Bigliani
Subacromial impingement is a common disorder of the shoulder that requires further investigation to understand the cause and treatment options. Knowledge of the pathogenesis of the condition has expanded greatly since Neer’s original ideas 40 years ago. In recent years, several different factors have been identified that contribute to impingement and rotator cuff disease. The purpose of this chapter is to discuss the mechanism behind subacromial impingement and emphasize new research about this disease, as well as treatment methods and their applications to the overhead athlete.
continued insult, stage II develops, identified by permanent histologic changes of fibrosis and tendinosis of the affected tendons. This is often the stage at which patients present to the orthopedic surgeon. If allowed to progress, stage III develops, with either a partial or complete rupture of the rotator cuff and biceps tendons and associated pathologic changes in the acromion and acromioclavicular joint. Stage III is not commonly seen in the general population younger than 40 years. However, in the overhead athlete, an individual may progress through each stage more rapidly. These patients can present with impingement pathology at an earlier age than usual. If left untreated for long periods, these shoulders may undergo chronic arthritic changes caused by unopposed superior migration of the humeral head into the acromion, a process known as cuff tear arthropathy. Stage II of outlet impingement, before the development of a complete rotator cuff tear, represents the population most frequently seen by orthopedic surgeons and will be the focus of this chapter.
CAUSES AND PATHOLOGY The cause of rotator cuff pathology has been the source of much controversy. Although rotator cuff tears were first described by Smith in 1834, disagreement remains as to which factors are principally responsible for this disease.1 Extrinsic factors, or the mechanical wear of the rotator cuff under the coracoacromial arch, have been described as the primary cause. Other intrinsic biologic forces, such as vascular supply to the tendons, aging, inflammation, and the development of degenerative tendinopathy have been identified as potential causes of external impingement. Studies have shed light on other factors that may lead to external compression injury, including poor posture, muscle weakness, subtle tissue contractures, and altered scapular or glenohumeral kinematics.2 Therefore, it is reasonable to conclude that the cause of subacromial impingement is variable and multifactorial.
As understanding of subacromial impingement has expanded, it has become clear that several mechanisms that contribute to rotator cuff injury may be occurring simultaneously. These mechanisms have been divided into two groups, intrinsic and extrinsic factors. Intrinsic causes represent overload, aging, and inflammatory processes that degrade the integrity of the tendons. Extrinsic injury represents direct compression. Compression under the coracoacromial arch, initially named by Neer as outlet impingement, is also known as subacromial impingement, classic impingement, or external impingement. More recently, another compression injury to the articular side of the rotator cuff and posterosuperior glenoid rim and humerus has been described, known as internal impingement (see Chapter 11).
Abnormal morphology of the acromion and the link to impingement syndrome were described by Neer in 1972. He isolated the undersurface of the anterior one third of the acromion rather than its lateral or posterior aspect as the area responsible for mechanical wear on the structures in the subacromial space. Neer identified the coracoacromial ligament and acromioclavicular joint as structures that also contribute to impingement on the rotator cuff.3,4
The acromion, coracoacromial ligament, and coracoid are the components of the coracoacromial arch. The coracoacromial arch superiorly and the humerus inferiorly serve as rigid boundaries for the soft tissue contents of the subacromial space. To achieve forward elevation above 90 degrees, the rotator cuff must pass under this arch. There is always contact between the cuff and arch, because the subacromial space is a relative space. Prior investigation has demonstrated anterolateral contact present at 0 degrees of elevation, which shifts medially with forward elevation. The humerus contacts the undersurface of the supraspinatus from proximal to distal with forward elevation. The primary point of contact on the bursal side is at the supraspinatus
The pathology may involve one or more of the rotator cuff tendons and the long head of the biceps. Neer outlined three progressive stages. Stage I is characterized by edema and hemorrhage of the subacromial bursa. Stage I usually occurs in younger patients and is difficult to distinguish from an acute partial tear of the rotator cuff without imaging studies. This stage is reversible with conservative treatment. With 115
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insertion throughout forward elevation. The subacromial bursa facilitates this motion and contact. It is a unique anatomic arrangement that exposes the soft tissues to wear and degeneration as the arm is elevated and rotated during range of motion of the shoulder. Furthermore, the impingement may be accelerated by any anatomic architectural changes in the acromion or acromioclavicular joint that reduce the volume of the subacromial space.
ANATOMY Normal Anatomy The development and function of the acromion are unique in humans. Studies of human embryos have shown that the acromion is identifiable by 5 or 6 weeks of age and is composed of cartilage at birth. The centers of ossification in the acromion, usually two, are the last to appear in the scapula; these appear during puberty or adolescence and usually fuse between 18 and 25 years of age.5,6 One variation that has been well outlined is failure of ossification, referred to as os acromiale. This anomaly may be present in up to 8% of cases and is often bilateral.7,8 The acromion is positioned above the superior aspect of the shoulder as the lateral extension of the spine of the scapula. It is defined posteriorly at the acromial angle, where the acromion and crest of the spine of the scapula converge. The posterior extent and lateral border of the acromion are easily defined with palpation. Anteriorly, at the tip, is the attachment of the coracoacromial ligament, where spur formation may be found. The coracoacromial ligament is located superior to the subacromial space. This ligament is a broad fan-shaped structure between the anterior aspect of the acromion and lateral tip of the coracoid. The acromioclavicular joint involves the medial aspect of the acromion and lateral aspect of the clavicle; it is the only diarthrodial articulation of the acromion. The opposing articular surfaces of the acromioclavicular joint may vary in their angulation when viewed anteriorly, and the surfaces are separated by an intra-articular disc in the early stages of life. Degeneration of the acromioclavicular joint occurs with age, and the formation of inferior osteophytes on the acromial or clavicular side increases in frequency with advancing years.9-11 The long head of the biceps and tendons of the rotator cuff pass through the subacromial space; these include the supraspinatus, infraspinatus, and teres minor muscles, which insert onto the greater tuberosity of the humerus. The subscapularis muscle inserts onto the lesser tuberosity. The rotator interval is created between the subscapularis and supraspinatus tendons. All four rotator cuff tendons interlace with each other over the humeral head before inserting. This continuity allows a functional interaction of the rotator cuff
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muscles and the ability to contribute to all motions of the glenohumeral joint. Subjacent to the anterior aspect of the supraspinatus lies the tendon of the long head of the biceps, which courses between the lesser and greater tuberosity in the bicipital groove. The subacromial bursa lies superior to the rotator cuff tendons, extending from the medial aspect of the acromion to the proximal one third of the humerus, underlying the deltoid muscle as it extends distally. The bursa is believed to have a lubricating effect by reducing friction of the rotator cuff under the coracoacromial (CA) arch. The vascular supply to the rotator cuff muscles and tendons includes contributions from the suprascapular, anterior and posterior humeral circumflex, thoracoacromial, and subscapular arteries. A region of hypovascularity in the supraspinatus tendon corresponds to the critical area, where rotator cuff pathology is usually initiated.12-15
Variations in Architecture Associated with Rotator Cuff Pathology Classically, external impingement occurs in the supraspinatus outlet as the arm is elevated from 70 to 120 degrees, also known as the impingement arc. It has been recognized that compression can occur at any point under this arch, and that processes that diminish the size or increase the rigidity of the outlet structures will exacerbate impingement.16 Conversely, measures taken to enlarge the outlet will relieve symptoms. The subacromial decompression enlarges the outlet in three ways: (1) by removing the prominent anterior acromion; (2) by releasing a tight coracoacromial ligament; and (3) by removing the bulky, thickened subacromial bursa. Prominent inferior osteophytes from the acromioclavicular joint may also contribute and are removed as necessary. Native anatomy can vary substantially. As Neer noted in his original paper on the subject, individual variation in the shape or slope of the acromion may affect the progression of impingement lesions.4 Bigliani and colleagues17 have studied the shape of the acromion in 140 cadaver shoulders to determine the relationship to full-thickness tears of the rotator cuff. The overall incidence of full-thickness tears in this elderly population was 34%. Three types of acromions were identified—type I (flat) in 17%, type II (curved) in 43%, and type III (hooked) in 39% (Fig. 10-1). The type III acromion was present in 70% of patients with rotator cuff tears, whereas only 3% of type I acromions were associated with a tear. Also, anterior acromial spurs were noted in 14% of those in the series overall but in 70% of patients with rotator cuff tears. It is important to distinguish between spurs, which are probably acquired, and variations of the native acromial architecture. Clinically, the same investigators examined acromial morphology using the supraspinatus outlet view in 200 consecutive patients with different shoulder problems.18
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A
B
C Figure 10-1. Variations of acromial morphology. A, Type I, flat. B, Type II, curved. C, Type III, hooked.
The incidence of acromial type correlated closely to the anatomic study—18% type I, 41% type II, and 41% type III. In patients with an arthrogram positive for a full-thickness rotator cuff tear, 80% had a type III acromion. In another group of 50 patients who underwent open subacromial decompression, 6% had a type I, 28% had a type II, and 66% had a type III acromion. Of this symptomatic group, 70% had a full-thickness rotator cuff tear. The findings of this study established a correlation between the type III acromion and rotator cuff tears and confirmed the importance of the supraspinatus outlet radiographic view for evaluation of the acromion. Other investigators have demonstrated a significant correlation between a hooked morphology and decreased Constant-Murley score.19 Other investigators have investigated the slope of the acromion.20 Aoki and coworkers21 have developed a technique for measuring the acromial slope using the supraspinatus outlet view of the scapula. Their investigation of skeletal shoulders has revealed that a flatter acromial slope may be associated with the presence of a spur and narrowing of the supraspinatus outlet. When applied clinically, patients with stage II impingement compared with normal patients had a significantly flatter acromial slope. In addition to acromial morphology, other anatomic factors have been associated with impingement of the rotator
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cuff. Many clinicians have described the occurrence of inferiorly protruding osteophytes from the anterior aspect of the acromion and inferior aspect of the acromioclavicular joint, which may compromise the integrity of the rotator cuff tendons when they pass below these structures.3,18,22 The anterior bony prominence, or traction spur, represents an enthesopathic reaction to the humerus repeatedly abutting the undersurface of the coracoacromial ligament. Chambler and colleagues23 have suggested that humeral contact from overhead motion causes rapid alterations in tension within the substance of the coracoacromial ligament that may provoke an adaptive change at the enthesis, leading to spur formation. Also, several series involving overhead athletes have suggested that the coracoacromial ligament is a primary source of pathology in this population. Suenaga16 has demonstrated in histologic studies that some patients have hypertrophic fibrocartilaginous changes within the coracoacromial ligament while having a normal-appearing acromial undersurface during arthroscopy. Soslowsky and associates24 have found that shoulders with rotator cuff tears have shortening and thickening of the anterolateral band of the coracoacromial ligament compared with shoulders with intact rotator cuff tendons. The subacromial bursa has also been implicated in the pathogenesis of rotator cuff disease and impingement. There is a rich supply of nerve fibers in the bursa compared with that in other tissues in the subacromial space, which may be responsible for the pain associated with impingement syndrome. Increased inflammatory cytokine expression has been identified in patients with subacromial bursitis compared with control patients. Developmental problems, such as failure of fusion of the acromial epiphyses, may alter the structure of the undersurface of the acromion and decrease the volume of the subacromial space.8,25,26 Although this may lead to bursal and rotator cuff lesions, coracoid impingement should be distinguished from the much more common form of subacromial, or outlet, impingement that typically is initiated in the supraspinatus tendon.
IMPINGEMENT IN THE ATHLETIC SHOULDER: PATHOPHYSIOLOGY AND CLINICAL CORRELATION Reports concerning injuries of the rotator cuff in athletes have increased tremendously during the past 30 years.27-38 There is a greater awareness about overuse syndromes and the impact that repetitive motions have on the rotator cuff, particularly those motions occurring above the horizontal plane. As a result, impingement and its pathophysiology have been well described in this population. Occasionally, the pathology is caused by an acute traumatic episode.37 Frequently, microtrauma to the subacromial bursa and
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rotator cuff tendons abutting the coracoacromial arch during repeated overhead motion will cause pain and a decrease or complete loss in function.29,33,34,38-41 Furthermore, involvement of the biceps tendon and the tendon’s association with impingement of the supraspinatus tendon have been well defined.4 The function of the rotator cuff muscles and motion of the shoulder in overhead sports have also been delineated.42,43 The rotator cuff muscles serve to compress the humeral head dynamically into the glenoid, providing stability during motion of the glenohumeral joint. The complex shoulder motions and the muscles involved in athletics have also been described in detail.44,45 In general, many overhead motions in sports, such as throwing a ball, serving in tennis, and swimming require maximal abduction with external rotation. This subjects subacromial bursa and rotator cuff tendons to wear under the anterior acromion and coracoacromial ligament as the arm accelerates forward. The bursa is a reactive membrane and this external mechanical stimulus may initiate a response of intrinsic factors, leading to inflammation and cuff disease. Impingement also may be seen if the rotator cuff muscles are weak and fail to stabilize the humeral head in the glenoid for proper mechanics. As a result, the action of the deltoid muscle will not be counterbalanced and the humeral head may translate superiorly into the coracoacromial arch. Tightness of the posterior capsule is known to limit glenohumeral internal rotation and create obligate anterior and superior humeral translation during flexion.46-48 Scapular mechanics also plays a role in some individuals in the contribution to subacromial impingement. Weakness of the dorsal scapular stabilizers and tightness of the pectoralis minor and short head of the biceps lead to scapular protraction and anterior tilting. This protracted and anteriorly tilted posture causes the scapula to tilt forward and places the acromion in a more horizontal position; thus, there is relative lowering of the roof of the coracoacromial arch and a decrease in the supraspinatus outlet space.49 Although extrinsic factors are a component of the disease, intrinsic factors have been demonstrated. Inflammatory mediators have been demonstrated by a number of researchers in both bursal and tendon tissues of patients with symptomatic impingement.50-53 Amyloid deposition has been demonstrated in patients with chronic pain, suggesting a degenerative component.54 Studies examining the stumps of torn tendons have demonstrated thinning and disorientation of collagen fibers, also suggesting a degenerative process.55 The debate among researchers as to whether rotator cuff disease is the result of an extrinsic mechanical force or an intrinsic problem within the tissue seems to indicate that multiple processes can be responsible at the same time. What seems likely is that repeated overhead motion in a
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constricting space mechanically presses the tissue and sets off a reaction that is inflammatory in nature. This increase in inflammatory mediators and cytokines has been demonstrated by various researchers. It is the contribution of mechanical and molecular factors to tissue weakened from previous insults that causes failure.
EVALUATION A complete evaluation, including a thorough history and physical examination, is required for all patients presenting with shoulder pain. Symptoms suggestive of impingement include pain with overhead activities, such as combing the hair and reaching high shelves. Pain with internal rotation is a common complaint. Night pain while lying on the affected side is also a frequent problem. Patients may locate the pain to the anterior shoulder or lateral deltoid, because the subacromial bursa extends beyond the lateral border of the acromion. Overhead athletes with impingement and cuff pathology secondary to subtle anterior instability are usually young and complain of pain and decreased throwing velocity. The physical examination should begin with inspection, looking for abnormal posture and signs of wasting or scapular winging that suggest neurologic injury or entrapment. The cervical spine should be examined, looking for evidence of degenerative disc disease, arthritis, or radicular pain. Range of motion is documented for forward elevation in the plane of the scapula, external rotation with the arm at the side and in 90 degrees of abduction, and internal rotation to the highest vertebral level. Ranges are compared with those of the contralateral shoulder. It is not unusual to see excessive external rotation in an overhead athlete, but with overall decreased range of rotation when compared with the nondominant extremity. Tests specific for impingement include Neer’s sign; this is measured by passively elevating the arm in the plane of the scapula while the examiner stabilizes the scapula with a hand. A positive test elicits pain between 70 and 120 degrees of elevation. Hawkins’ test is performed with the shoulder flexed 90 degrees and internally rotated (Fig. 10-2). Anatomic studies have validated both tests for placing the rotator cuff in contact with the undersurface of the coracoacromial arch and clinical studies have confirmed their high sensitivity, although specificity is low.56 The sensitivity of Hawkins’ test was 92% in two independent studies.57,58 Not to be confused with his impingement sign, Neer’s impingement test involves the injection of 10 mL of lidocaine into the subacromial space, followed by performance of the provocative motion. A positive test will relieve pain in those with impingement and calcific tendinitis but will continue to be painful if other causes are responsible. This test has been shown to be an independent predictor of good outcome after arthroscopic subacromial decompression.59,60
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Figure 10-2. Hawkins’ impingement test.
Figure 10-3. Scapular Y view demonstrating anterior spur.
Patients with impingement generally have good ranges of motion and strength. A positive drop arm test, liftoff test, hornblower’s sign, and external and internal rotation lag signs should alert the clinician to a complete rotator cuff tear. Significant loss of passive range of motion is a feature of adhesive capsulitis, not primary impingement, although the two may coexist. Subtle instability can be detectable through a positive relocation test on examination.
axial view is good for identifying bicep tendon and subscapularis pathology.
When treating an athlete with impingement syndrome, the anatomy of the coracoacromial arch should be considered as part of the evaluation. Radiographic evaluation can identify any bony abnormality or spur that may be the source of the pathology. Spur formation usually occurs in older patients older than 40 years, but we have seen them in younger overhead athletes who compress the humerus and cuff against the coracoacromial ligament. Spur formation occurs in the insertion of the coracoacromial ligament into the undersurface of the acromion. Diagnostic studies include the anteroposterior (AP) view in the plane of the scapula and supraspinatus outlet and an axillary lateral view. The AP view helps distinguish between other sources of pain, such as calcific tendinitis and arthritis. The supraspinatus outlet view can alert the clinician to altered acromial morphology or acromial spurs (Fig. 10-3). The axillary lateral view can demonstrate an os acromiale if present. In the early stages, routine magnetic resonance imaging (MRI) is not recommended. However, if symptoms persist or if significant rotator cuff pathology is suspected by clinical examination, MRI is recommended. MRI is useful to identify inflammation. The coronal and sagittal oblique views will demonstrate bursitis and cuff pathology (Fig. 10-4). Acromial morphology, such as the presence of a spur or failure of formation, can be better identified as well. The
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TREATMENT The initial management of a patient with subacromial impingement is conservative. Avoidance of provocative activities, anti-inflammatory medication, and physical therapy should be the initial modes of treatment.60 Physical therapy
Figure 10-4. Sagittal oblique magnetic resonance imaging scan demonstrating anterior spur and inflamed bursa.
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plays an integral role in the treatment of impingement, both in preventing surgery and for postoperative rehabilitation. Conservative measures in patients with type I acromions had a success rate of 89% in one series.61 Targeted therapy on scapular stabilizers and humeral head compressors has been shown to improve range of motion and decrease pain significantly.62 Traditionally, only anecdotal evidence existed regarding steroid injections for the treatment of impingement. Their effectiveness in the short term has now been validated in randomized, double-blinded clinical studies.63 However, the accuracy of injection placement has come into question, with one study demonstrating that only 70% of injections reach the subacromial space, as verified by bursography.64 Furthermore, there is little information about the content of the injections and the efficacy of different synthetic steroids. We prefer a combination of 2 mL of methylprednisolone (Depo-Medrol), 4 mL of 1% lidocaine, and 4 mL of 0.25% bupivacaine (Marcaine) injected through the anterior or posterolateral portal site. Although there are no quantitative data, it is generally believed that repeated injections should be avoided because of the potentially adverse effects on tendon integrity.65,66
Surgical Treatment As Neer solidified his theory of impingement, he advocated the anterior acromioplasty, recognizing that only a small anterior portion of bone is involved. This procedure remains the basis for how treatment is carried out today. The main advantages of the anterior acromioplasty are limited removal of bone and greater preservation of the deltoid muscle origin. The treatment of impingement in an older patient also includes the débridement of the subacromial bursa, coracoacromial ligament release and, if necessary, resection of osteophytes at the acromioclavicular joint. Ellman first described performing this operation through the arthroscope in 1985.67 The follow-up in this study reported good to excellent results in 88% of patients based on the UCLA shoulder rating scale. Since that time, prospective randomized studies comparing open with arthroscopic acromioplasty have found both methods to be reliable, with only minor differences.68-70 The role of the coracoacromial ligament in impingement has been given more attention in the athlete (Fig. 10-5). Most overhead motions in sports begin with abduction and external rotation, followed by forward flexion and internal rotation. With repetition of these motions, pain and decreased function may result from mechanical wear on the bursa and rotator cuff as they pass below the leading edge of the coracoacromial ligament and anterior acromion. Surgical resection of the coracoacromial ligament without acromioplasty has uniformly provided these patients with pain relief, but has not allowed most of those athletes to return to their previous level of function.71 This phenomenon has been
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Figure 10-5. Coracoacromial ligament.
noticed particularly in pitchers. The less than ideal outcome following isolated coracoacromial ligament resection and decompression should not imply that the addition of an anterior acromioplasty will lead to an improved outcome in these patients. Tibone and colleagues39 have studied 45 athletes with incomplete or complete rotator cuff tears; they found that 80% of patients with incomplete tears treated with an anterior acromioplasty have improved pain relief, but an overall good result was seen in only 50%. More recent long-term studies by Stephens and associates have reported the 6- to 10-year follow-up of arthroscopic acromioplasty for chronic impingement; 81% of patients had good to excellent results. However, one third of athletes were not able to return to overhead and throwing sports. It was hypothesized that occult instability may have been a factor in these patients and suggests ruling this out before surgery; it was also suggested that throwers be considered as a separate clinical group from the general population with impingement. In the athletic population, anterior instability follows impingement pathology as the second most common shoulder problem.40 Instability may lead to subluxation of the humeral head, causing mechanical impingement secondarily. Whether or not impingement is the primary or secondary cause for rotator cuff pathology in an athlete with shoulder pain, early intervention with a specifically designed rehabilitation program can alleviate symptoms and restore function.36,72,73 It is our recommendation that true impingement in the older athlete be treated with bursectomy, limited anterior acromioplasty, and CA ligament resection (Fig. 10-6). In young overhead athletes with isolated impingement, bursectomy and partial longitudinal anterior band CA ligament resection should be performed without acromioplasty.
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A
B Figure 10-6. Coracoacromial ligament excision. A, Defining the spur. B, Post–spur excision.
SUMMARY Variations in the architecture of the coracoacromial arch can lead to a clinically symptomatic rotator cuff lesion. Differences in the shape and slope of the acromion and the presence of anterior acromial spurs or inferior protruding acromioclavicular osteophytes may decrease the volume of the subacromial space, leading to impingement. Treatment should be focused initially on nonoperative modalities, such as rest, anti-inflammatory medications, and physical therapy, with surgical decompression used as a final option.
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7. Grant JCB: The upper limb. In Grant JCB (ed): A Method of Anatomy, 2nd ed. Baltimore, Williams & Wilkins, 1940. 8. Lieberson E: Os acromiale: A contested anomaly. J Bone Joint Surg 19:683, 1937. 9. DePalma AF: Surgical anatomy of acromioclavicular and sternoclavicular joints. Surg Clin North Am 43:1541, 1963. 10. Moseley HF: The clavicle and its articulations. In Moseley HF (ed): Shoulder Lesions, 2nd ed. New York, Hoeber, 1953. 11. Petersson CJ: Degeneration of the acromioclavicular joint: a morphological study. Acta Orthop Scand 54:434, 1983. 12. Lindblom K: On pathogenesis of ruptures of the tendon aponeurosis of the shoulder joint. Acta Radiol 20:563, 1939. 13. Moseley HF, Goldie I: The arterial pattern of the rotator cuff of the shoulder. J Bone Joint Surg Br 45:780, 1963. 14. Rathbun JB, Macnab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52:540, 1970. 15. Rothman RH, Parke WW: The vascular anatomy of the rotator cuff. Clin Orthop Relat Res 41:176, 1965. 16. Suenaga N: The correlation between burscopic and histologic findings of the acromion undersurface in patients with subacromial impingement syndrome. Arthroscopy 18:16, 2002. 17. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228, 1986. 18. Morrison DS, Bigliani LU: The clinical significance of variations in acromial morphology. Orthop Trans 11:234, 1987. 19. Constant CR, Murley AH: A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res 214:160, 1987. 20. Aoki M, Ishii I, Usui M: The slope of the acromion and rotator cuff impingement. Orthop Trans 10:228, 1986. 21. Aoki M, Ishii I, Usui M: Clinical application for measuring the slope of the Acromion. In Post M, Hawkins RJ, Morrey BF (eds): Surgery of the Shoulder. St. Louis, Mosby Year Book, 1990, pp 200. 22. Petersson CJ, Gentz CF: Ruptures of the supraspinatus tendon: The significance of distally pointing acromioclavicular osteophytes. Clin Orthop Relat Res 174:143, 1983. 23. Chambler AF, Pitsillides AA, Emery RJ: Acromial spur formation in patients with rotator cuff tears. J Shoulder Elbow Surg 12:314, 2003. 24. Soslowsky LJ, An CH, Johnston SP, Carpenter JE.: Geometric and mechanical properties of the coracoacromial ligament and their relationship to rotator cuff disease. Clin Orthop Relat Res 304:1, 1994. 25. Bigliani LU, Norris TR, Fischer J, et al: The relationship between the unfused acromial epiphysis and subacromial lesions. Orthop Trans 7:138, 1983. 26. DePalma MJ, Johnson EW: Detecting and treating shoulder impingement syndrome. Phys Sport Med 31:25, 2003. 27. Bateman JE: Cuff tears in athletes. Orthop Clin North Am 1:721, 1973. 28. Bigliani LU, D’Alessandro DF, Duralde XA, et al: Anterior acromioplasty for subacromial impingement in patients younger than 40 years of age. Clin Orthop Relat Res 246:111, 1989. 29. Cofield RH, Simonet WT: The shoulder in sports. Mayo Clin Proc 59:157, 1984. 30. Fowler P: Swimmer problems. Am J Sports Med 7:141, 1979. 31. Fu FH, Harner CD, Klein AH: Shoulder impingement syndrome: A critical review. Clin Orthop Relat Res 269:162, 1991.
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32. Gainor BJ, Piotrowski G, Puhl J, et al: The throw: biomechanics and acute injury. Am J Sports Med 8:114, 1980. 33. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 34. Jackson DW: Chronic rotator cuff impingement in the throwing athlete. Am J Sports Med 4:231, 1976. 35. Jackson DW: Problems among the inexperienced and experienced athlete. Am J Sports Med 7:142, 1979. 36. Jobe FW: Impingement problems in athletes. ICLS 38:205, 1989. 37. Neer CS, Welsh RP: The shoulder in sports. Orthop Clin North Am 8:583, 1977. 38. Penny JN, Welsh RP: Shoulder impingement syndromes in athletes and their surgical management. Am J Sports Med 9:11, 1981. 39. Tibone JE, Elrod B, Jobe FW, et al: Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am 68:887, 1986. 40. Jobe FW, Jobe CM: Painful athletic injuries of the shoulder. Clin Orthop Relat Res 173:117, 1983. 41. Norwood LA, Del Pizzo W, Jobe FW, et al: Anterior shoulder pain in baseball pitchers. Orthop Trans 2:20, 1978. 42. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220, 1988. 43. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247, 1983. 44. Jobe FW, Tibone JE, Perry J, et al: An EMG analysis of the shoulder in throwing and pitching: A preliminary report. Am J Sports Med 11:3, 1983. 45. Tullos HS, King JW: Throwing mechanism in sports. Orthop Clin North Am 1:709, 1973. 46. Tyler TF: Quantification of posterior capsule tightness and motion loss in patients with subacromial impingement. Am J Sports Med 28:668, 2000. 47. Harryman DT: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334, 1990. 48. Graichen H: Three-dimensional analysis of shoulder girdle and supraspinatus motion patterns in patients with impingement syndrome. J Orthop Res 19:1192, 2001. 49. Solem-Bertoft E, Thuomas KA, Westerberg CE: The influence of scapular retraction and protraction on the width of the subacromial space: An MRI study. Clin Orthop Relat Res 296:99, 1993. 50. Sakai H: Immunolocalization of cytokines and growth factors in subacromial bursa of rotator cuff tear patients. Kobe J Med Sci 47:25, 2001. 51. Yoshida M: Pathologic gene expression in adhesive subacromial bursae of the human shoulder. Clin Orthop 412:57, 2003. 52. Yanagisawa K: Vascular endothelial growth factor expression in the subacromial bursa is increased in patients with impingement syndrome. J Orthop Res 19:448, 2001. 53. Blaine TA, Kim YS, Voloshin I, et al: The molecular physiology of subacromial bursitis in rotator cuff disease. J Shoulder Elbow Surg 14(Suppl S):84S, 2005.
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54. Cole AS: Localized deposition of amyloid in tears of the rotator cuff. J Bone Joint Surg Br 83:561, 2001. 55. Hashimoto T, Nobuhara K, Hamada T: Pathologic evidence of degeneration as a primary cause of rotator cuff tear. Clin Orthop Relat Res 415:111, 2003. 56. Valadie AL: Anatomy of provocative tests for impingement syndrome of the shoulder. J Shoulder Elbow Surg 9:561, 2001. 57. MacDonald PB, Clark P, Sutherland K: An analysis of the diagnostic accuracy of the Hawkins and Neer subacromial impingement signs. J Shoulder Elbow Surg 9:299, 2000. 58. Calis M: Diagnostic values of clinical diagnostic tests in subacromial impingement syndrome. Ann Rheum Dis 59:44, 2000. 59. Mair SD: Can the impingement test predict outcome after arthroscopic subacromial decompression? J Shoulder Elbow Surg 8:231, 1999. 60. Morrison DS, Frogameni AD, Woodworth P: Non-operative treatment of subacromial impingement syndrome. J Bone Joint Surg Am 79:732, 1997. 61. Wang JC: The relationship between acromial morphology and conservative treatment of patients with impingement syndrome. Orthopaedics 23:557, 2000. 62. Walther M: The subacromial impingement syndrome of the shoulder treated by conventional physiotherapy, self-training, and a shoulder brace: Results of a prospective, randomized study. J Shoulder Elbow Surg 13:417, 2004. 63. Blair B: Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 78:1685, 1996. 64. Yamakado K: The targeting accuracy of subacromial injection to the shoulder: An arthrographic evaluation. Arthroscopy 18:887, 2002. 65. Akpinar S: Effects of methylprednisolone and betamethasone injections on the rotator cuff: An experimental study in rats. Adv Ther 19:194, 2002. 66. Tillander B: Effect of steroid injection on the rotator cuff: An experimental study in rats. J Shoulder Elbow Surg 8:271, 1999. 67. Ellman H: Arthroscopic subacromial decompression: Analysis of one- to three-year results. Arthroscopy 18:173, 1987. 68. Husby T: Open versus arthroscopic subacromial decompression: A prospective, randomized study of 34 patients followed for 8 years. Acta Orthop Scand 74:408, 2003. 69. Spangehl MJ: Arthroscopic versus open acromioplasty: A prospective, randomized blinded study. J Shoulder Elbow Surg 11:101, 2002. 70. Lindh M, Norlin R: Arthroscopic subacromial decompression versus open acromioplasty. A two-year follow-up study. Clin Orthop Relat Res 290:174, 1993. 71. Tibone JE, Jobe FW, Kerlan RK, et al. Shoulder impingement syndrome in athletes treated by anterior acromioplasty. Clin Orthop Relat Res 198:134, 1985. 72. Pappas AM, Zawacki RM, McCarthy CF: Rehabilitation of the pitching shoulder. Am J Sports Med 13:223, 1988. 73. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10:336, 1982.
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CHAPTER 11 Internal Impingement Michael M. Reinold, Kevin E. Wilk, Jeffrey R. Dugas, and James R. Andrews
Internal impingement is one of the most common shoulder pathologies seen in overhead athletes. Walch and colleagues1 first described internal impingement as contact between the articular side of the supraspinatus and/or infraspinatus tendon and the posterosuperior rim of the glenoid when the arm is abducted to 90 degrees and externally rotated, as seen during the late cocking and early acceleration phases of the overhead throwing motion (Fig. 11-1). This pathology differs from classic shoulder impingement, as described by Neer,2,3 which involves contact between the bursal side of the rotator cuff, usually the supraspinatus tendon, and the coracoacromial arch during arm elevation. Walch and coworkers1 noted this contact of the tendon in this area in 17 overhead athlete patients; Andrews and associates4 described this undersurface rotator cuff fraying in overhead athletes almost a decade earlier and, at the time, it was hypothesized that these lesions occur from excessive traction on the cuff from repetitive throwing.
Anatomic Theory Several authors have shown that there is contact between the posterior rotator cuff and glenoid rim and labrum with abduction and external rotation of the shoulder, which has been theorized to be a normal occurrence for the overhead athlete. Jobe and Sidles5 have demonstrated this on cadaver shoulders. Using magnetic resonance imaging (MRI), Halbrecht and colleagues6 have examined 10 asymptomatic college baseball pitchers in the abducted externally rotated position. All 10 pitchers demonstrated contact of the rotator cuff on the posterosuperior glenoid on the throwing shoulder; however, none exhibited this contact on the nonthrowing shoulder. It is still unknown whether contact itself is the same as pathologic internal impingement. The rationale for this theory of why contact occurs on the throwing shoulder and not the other side may be caused by bilateral anatomic differences in range of motion, laxity, humeral retroversion, or a combination of these factors. All these characteristics have been shown to be altered on the dominant side of overhead athletes (see later). Although contact has been shown to occur in the asymptomatic athlete, it is still unknown whether this is a normal occurrence in all overhead athletes or if the subjects involved in the studies cited demonstrated the specific characteristics that predispose the athlete to internal impingement. It is possible that contact of the rotator cuff on the glenoid is a normal occurrence in the overhead athlete because of the unique anatomic characteristics of the thrower’s shoulder. Consequently, with chronic repetitive contact, symptomatic internal impingement may arise as articular-sided rotator cuff partial tearing and labral pathology develop, after concomitant injuries to the labrum and capsule that affect the static stability of the shoulder, or both.
Since this original description, several theories have been proposed and new research has shed light on the mechanisms and consequences of internal impingement. The repetitive contact (or rubbing) between the tendon and glenoid rim during the throwing motion has been shown to result in undersurface partial-thickness rotator cuff tearing, posterosuperior glenoid labrum fraying or detachment, and cystic changes on the posterolateral aspect of the humeral head. Internal impingement, once considered simply impingement of the undersurface of the rotator cuff on the glenoid rim, now encompasses a broad spectrum of interrelated pathologies, including partial-thickness, articularsided, rotator cuff tears, capsular instability, superior labral anterior-posterior (SLAP) lesions, and occasional humeral head cystic changes. The purpose of this chapter is to discuss the pathology and pathomechanics of internal impingement. Using this background, we will review the examination, surgical intervention, and rehabilitation principles of caring for the athlete with internal impingement.
Anterior Laxity Theory The second proposed theory is the anterior laxity or instability theory. The anterior capsule undergoes significant tensile stress in the late cocking and early acceleration phases of the throwing motion. This stress can lead to gradual stretching of the capsular collagen over time, leading to increased anterior capsular laxity. Several clinicians7-11 have proposed that this repetitive strain on the anterior capsule in overhead athletes causes anterior capsular laxity over time. Mihata and associates12 have demonstrated in the cadaveric model that excessive external rotation (ER)
PATHOLOGY Numerous theories have been proposed to explain internal impingement in the overhead athlete. We will briefly discuss these theories, with the current scientific rationale for each. 123
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colleagues14 have subsequently shown that increasing the capsular elasticity by 30% produces an increase in external rotation of 18 degrees. Regardless of the answer, there is little doubt that increased anterior capsular laxity produces significant changes in the biomechanics of the shoulder throughout the throwing motion. Jobe15 and Davidson and associates16 have also described how improper throwing mechanics may also play a role in increasing anterior translation. Hyperangulation (excessive horizontal abduction), or opening up during the acceleration phase, causes the humerus to move posteriorly to the plane of the scapula, which may lead to increased strain on the anterior structures (Fig. 11-2).
Figure 11-1. Internal impingement. Shown is articular-sided impingement of the infraspinatus and/or supraspinatus on the posterosuperior glenoid rim.
If increases in anterior capsular laxity can lead to internal impingement, can reversing such changes decrease the likelihood of injury? This clinical question remains to be answered. Alberta and coworkers17 have measured rotation and translation in six intact cadaveric specimens. Measurements were repeated after stretching the anterior capsule and after plicating the anterior capsule in an attempt to reproduce the normal condition. It was found that with stretching of the anterior capsule, increased external rotation results, without a resultant posterior superior migration. Plication subsequently reduces external rotation and anterior translation, along with moving the center of rotation posteriorly and inferiorly (away from the rotator cuff and labrum) in external rotation.
results in elongation of the anterior band of the inferior glenohumeral ligament complex. Consequently, a significant increase in anterior and inferior capsular translation is noted. This acquired laxity from repetitive throwing may not manifest as gross anterior instability, although it is commonly believed that microinstability may be present (see later). This has been theorized to allow the humeral head to translate anteriorly during the cocking phase of throwing. Even if the amount of anterior translation is negligible, any further anterior displacement may cause—or increase—the undersurface of the posterior rotator cuff musculature to impinge on the posterosuperior glenoid rim. Thus, any amount of increased anterior translation may amplify the amount of internal impingement observed.
Posterior Capsular Tightness Theory Another theory is the posterior glenohumeral capsular tightness theory, proposed by Burkhart and colleagues,18 who hypothesized that the posterior capsule may become tight, causing a loss of glenohumeral internal rotation and posterosuperior humeral head translation. To date, no clinical data have shown this to be present. These researchers
A common debate among experienced clinicians centers around which occurs first, the increase in external rotation or the increase in capsular laxity. Fitzpatrick and coworkers13 have demonstrated that with increased capsular laxity, increases in external rotation occur. Schneider and Scapular axis
Scapular axis
o o –40
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Figure 11-2. Hyperangulation of the shoulder during throwing. A, Arm in the scapular plane. B, Arm posterior to the scapular plane.
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o
Arm axis
o 40 30 –
Body axis
A
Body axis
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Arm axis
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coined the term glenohumeral internal rotation deficit (GIRD), which means that in the throwing shoulder, the athlete demonstrates a loss of 20 degrees or more of internal rotation compared with the opposite (nonthrowing) shoulder. The unique range-of-motion (ROM) characteristics of the shoulder in overhead throwing athletes have been well defined.11,19-26 These studies have shown that asymptomatic baseball pitchers normally exhibit increased ER and decreased internal rotation (IR) at 90 degrees abduction in the throwing shoulder. Wilk and associates11 have studied the shoulder passive ROM characteristics in 372 professional baseball players. They reported a mean of 129 ± 10 degrees of ER and 61 ± 9 degrees of IR in the throwing shoulder at 90 degrees abduction. It was noted that ER is 7 degrees more and IR 7 degrees less in the dominant arm when compared with the nondominant arm. The concept of total motion was introduced in this study; this is the total value of external and internal rotation ROM (at 90 degrees abduction) added together (Fig. 11-3). It was also noted that there is no significant difference in total motion bilaterally, despite alterations in external and internal rotation. These ROM characteristics have been shown in studies by several clinicians in baseball20-22 and tennis players.24
IR
ER
IR
ER Figure 11-3. Total motion concept. The overhead athlete presents with excessive external rotation (ER) and a limitation of internal rotation (IR). This same arc is present on the nondominant shoulder, but is shifted toward internal rotation.
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It is well recognized and reported that ROM adaptations are normal in the overhead throwing athlete. However, the precise cause of this adaptation has not been established. Several clinicians have documented humeral retroversion in the thrower’s shoulder and attribute the altered ROM to bony adaptations.23,27,28 Crockett and coworkers23 have demonstrated that the average humeral retroversion in asymptomatic throwers is almost 40 degrees, whereas symptomatic throwers have an average of only 24 degrees of retroversion. Thus, the bilateral difference in retroversion is 16 degrees. Athletes who have never participated in throwing sports have an average bilateral humeral retroversion of 24 degrees, which is equal bilaterally. Meister and colleagues26 have shown that the maximum increases in humeral retroversion occur between ages 12 and 13 years. Thus, it appears that the loss of IR in baseball players may be a normal occurrence caused by humeral retroversion as the athlete is developing. Clinically, it is our belief that a loss of IR or GIRD is not problematic, regardless of the differential amount of IR bilaterally, if total motion is equal bilaterally. However, if there is a loss of total motion and IR, we think that the athlete may be more susceptible to injury. Reinold and associates29 have recently analyzed ROM before and after pitching and noted that the throwing shoulder has a significant decrease of IR and total motion (⫺10 degrees for both) immediately after pitching. These changes are still present 24 hours after pitching. Furthermore, there are no significant changes on the nondominant shoulder. The acute loss of motion was attributed to microscopic muscle damage caused by eccentric contractions of the posterior shoulder musculature. Eccentric muscular contractions have been correlated with a rise in passive muscular tension and a loss of joint ROM.30 It is our experience that baseball players often describe generalized tightness in the musculature of their posterior shoulder after pitching. The muscles responsible for ER of the shoulder exhibit high eccentric muscle activity31-34 during the throwing motion as the shoulder internally rotates between 6000 and 7000 deg/sec.35-37 Previous studies examining the effect of repetitive eccentric contractions have shown a subsequent loss of joint ROM in the upper and lower extremities following testing.39-41 The theory of posterior capsular tightness has also been questioned by other researchers20,21 who have found that ROM in baseball pitchers, specifically a loss of IR, does not correlate with an alteration in posterior glenohumeral translation. Borsa and coworkers20 have studied glenohumeral translation in a series of 43 healthy professional baseball pitchers. They reported that posterior translation is twice that of anterior translation. There is also no difference between the amount of translation of the dominant and nondominant shoulder. However, they were unable to show a correlation between IR range of motion and posterior laxity.
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Thus, it appears that a loss of IR on the throwing shoulder is normal and related to a certain degree of bony retroversion. The eccentric muscle activities involved in baseball pitching may be responsible for an acute loss of IR immediately following pitching. It does not appear that players with a significant decrease in IR on the dominant shoulder have an associated loss of posterior glenohumeral translation. Currently, it is difficult to say whether posterior capsular tightness occurs in overhead athletes or this plays a role in internal impingement. Further research is required to explore this theory in greater detail.
Microinstability–Over-rotation Theory Another theroy represents a combination of the theories discussed, which all relate to microinstability and overrotation of the throwing shoulder. This theory states that internal impingement is a mixture of several pathologic entities, including partial-thickness, articular-sided, rotator cuff tearing and superior labral degeneration and tearing (SLAP tears), which are a result of a combination of capsular microinstability, excessive external rotation, and humeral retroversion. Although contact of the undersurface of the rotator cuff may be a normal anatomic occurrence, any concomitant microinstability, rotator cuff weakness, or other loss of static or dynamic stability from the act of throwing may facilitate the development of pathologic internal impingement. This would explain why internal impingement is only seen on the dominant throwing side and not on the nonthrowing shoulder. As previously noted, macroinstability, or dislocation, is distinctly uncommon in the overhead throwing athlete. Microinstability may be defined as any rotational or directional pathologic laxity that leads to abnormal mechanics within the shoulder, without frank dislocation. Such rotational or directional laxity can lead to partial rotator cuff tearing, labral detachment or fraying, further capsular damage, or combinations of these injuries. It has been theorized that repetitive pitching causes acquired anterior laxity as the anterior capsule undergoes significant stress. If the repetitive strain on the anterior capsule from pitching causes an increase in anterior microinstability, internal impingement is likely to occur. Rizio and colleagues42 have recently studied the effects of anterior capsular laxity on superior labral strain. They simulated anterior instability in the cadaveric model and noted that posterosuperior labral strain increases significantly by 160% during the late cocking phase of throwing in shoulders with anterior instability. As noted, even though there are significant differences in external rotation, the total arc of motion of the throwing shoulder is not significantly different from that of the nonthrowing shoulder. In the throwing shoulder, the total arc is spun back into an externally rotated position. The cause
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of this spin back is likely a combination of soft tissue and bony adaptive changes, including humeral retroversion, which occur in the thrower’s shoulder over many years. These findings have led various clinicians to conclude that bony adaptations are potentially protective against internal impingement in the throwing athlete. In other words, if a throwing shoulder does not develop the protective osseous retroversion, the anterior capsule must stretch to accommodate the requirements of throwing, leading to anterior capsular stretch and internal impingement. Thus, it is our opinion that it is important to identify players who do not have a spin back total arc of motion, because they may have decreased retroversion and be predisposed to developing anterior microinstability and internal impingement. Several theories have been discussed whose conclusions, in all likelihood, have a certain effect on the development of internal impingement. Regardless, it appears that the term internal impingement itself should be considered as a collective group of findings, including articular-sided rotator cuff partial tearing, superior labral degeneration and tearing, and other associated pathologies.
EXAMINATION Clinical examination of the athlete with internal impingement includes a standard shoulder evaluation (see Chapters 3 and 4). We will describe some components of the examination that are important to discuss when dealing with players with internal impingement. Because of associated pathologies, the clinical examination of the thrower with internal impingement should include assessments of range of motion, capsular laxity, superior labrum, and static and dynamic stabilizers of the shoulder. The injured thrower with internal impingement generally presents with pain while throwing. Subjectively, the player may complain that it is “difficult to warm up” or “get loose.” There is often a loss of velocity and lack of command while pitching. Common complaints in throwers with internal impingement include pain during the late cocking and early acceleration phases of throwing. This pain is often posterosuperior but can also be anterior or even vague in nature because of the combination of pathologies typically present with internal impingement. Pain to palpation at the posterior glenohumeral joint line is also a common physical examination finding. These symptoms, while throwing, can be re-created on physical examination using the internal impingement sign as described by Meister and associated.43 With the athlete supine, the arm is passively abducted to 90 degrees and maximally externally rotated, similar to a classic apprehension test. This maneuver is designed to rotate the humeral head into the position of internal impingement, re-creating symptoms. In this position, the athlete will experience
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discomfort in the posterosuperior aspect of the shoulder and often report a vague deep discomfort. This internal impingement sign is considered positive if relocation of the humeral head causes a decrease in symptoms (Fig. 11-4). This is performed by exerting a posterior force on the humeral head similar to the apprehension or relocation test for anterior instability. The fact that this relocation test is indicative of internal impingement lends credibility to the theory that anterior capsular laxity and microinstability are likely contributing factors to internal impingement. Establishing the athlete’s passive ROM is also important. Asymptomatic throwers should display total motion that is equal bilaterally. It is important to note whether a player has an increase or decrease in total motion. As noted, chronic repetitive eccentric muscle trauma of the posterior rotator cuff from pitching may result in a loss of internal rotation and sometimes horizontal adduction. If a player has a significant increase in total motion in comparison with his nondominant shoulder, the athlete probably has a certain degree of laxity present. Thus, examination of the athlete’s static stabilizers is important. The typical capsular examination is performed with the athlete supine. This includes drawer and fulcrum testing at 90 degrees of abduction. In addition to side to side differences, the end feel of the ligamentous restraints to translation should be noted. Because of the close association of superior labral pathology, testing for SLAP tears should also be conducted. It is our opinion that testing for SLAP tears in the overhead athlete should include special tests that reproduce the thrower’s motion and the peel-back mechanism, which include the supinated external rotation,45 pronated load,44 and biceps load tests.46,47 Often, other SLAP tests that do not reproduce the peel-back mechanism, such as the
A
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O’Brien test, may not reveal the pathology present or may produce a false-positive test because of rotator cuff overload in this provocative position. Most throwers exhibit a typical muscular strength pattern in the throwing shoulder. Wilk and colleagues48,49 using isokinetic testing, have reported that the thrower’s shoulder’s external rotators were approximately 5% to 7% weaker than those of the nonthrowing shoulder. The internal rotators were 15% to 20% stronger. The ER/IR unilateral ratio was 66% to 72% Athlete’s with internal impingement will often exhibit weakness with external rotation and full or empty can testing. Scapula position may also have an effect on range of motion. It has been reported that the thrower exhibits a dropped shoulder and scapula on the throwing side. Basten and associates50 have reported that the thrower scapula exhibits a more protracted and anteriorly tilted posture at rest when compared with the opposite side. Macrina and coworkers51 have noted that following throwing and fatigue, the throwing shoulder’s scapula exhibits greater protraction and anterior tilting compared with that before throwing. This anteriorly tilted posture may contribute to the loss of internal rotation exhibited by the thrower.
RADIOGRAPHIC DIAGNOSIS From a diagnostic standpoint, each patient should undergo standard throwers’ series plain radiography, including AP views, internal and external rotation, and West Point, axillary, and subacromial outlet views. MRI is used for the confirmation of suspected shoulder pathology. In the vast majority of throwers, the diagnosis of labral pathology is made on the basis of clinical history and physical
B
Figure 11-4. Internal impingement sign. The examiner passively positions the arm into external rotation (A) and pain is felt posterosuperiorly. The examiner may then exert a force on the anterior shoulder to relocate the shoulder (B) and symptoms are diminished.
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examination. Sophisticated and sensitive radiographic tests such as MRI are used to confirm the suspected pathology. The use of MRI for diagnostic purposes has increased in popularity in recent years, and the accuracy of these tests are highly correlated with the experience of the radiologist reading the results and the quality of the examination itself. As with any MRI, the strength of the magnet is one of the determinants of image quality. The use of intra-articular contrast increases the accuracy of diagnosis in the hands and eyes of many clinicians. Figure 11-5 shows the typical appearance of a type II SLAP lesion on contrast-enhanced MRI. Figure 11-6 shows the ABER (abduction external rotation) view, which is done with the arm in the position of internal impingement. This sequence of images is particularly useful in throwers with symptoms of internal impingement—posterior superior shoulder pain in the late cocking and early acceleration phases of throwing.
TREATMENT Nonoperative Management Nonoperative management of internal impingement is the primary treatment for this pathology, and is successful in the vast majority of cases. The rehabilitation program is a multiphase sequential approach. The athlete is initially instructed to abstain from throwing, generally from 2 to 6 weeks, depending on the severity and chronicity of symptoms. In the acute phase, the patient presents with the main complaint of pain and possible stiffness. In addition, the patient exhibits loss of motion and weakness of
Figure 11-6. ABER (abduction external rotation) view demonstrating internal impingement. The typical undersurface fraying that occurs in the infraspinatus can be seen.
the external rotators and specific scapular muscles. In this phase, treatment is focused on diminishing pain and inflammation. A common modality that we have found to be effective is iontophoresis using a long-duration patch such as the Empi Action Patch (Empi, St. Paul, Minn) or Hybresis patch (IOMED, St. Paul, Minn). Phonophoresis, ice, and nonsteroidal anti-inflammatory drugs (NSAIDs) may be used to reduce pain and inflammation as well. The athlete often exhibits a loss of internal rotation motion and horizontal adduction. We believe this internal rotation deficit is caused by inflammation and tightness of the external rotators and posterior musculature. The stretches we have athletes perform include the sleeper stretch (Fig. 11-7), supine horizontal adduction stretch (Fig. 11-8), supine horizontal adduction with internal rotation (Fig. 11-9), and passive ROM into internal rotation (Fig. 11-10). These stretches can be aggressive on the rotator cuff and should be performed in a controlled fashion. A sensation of stretching should be felt in the posterior aspect of the shoulder, not at the rotator cuff insertion. The goals of these stretches are to restore the athlete’s normal spun back total motion in comparison with the nonthrowing shoulder and to improve the athletes’ end range elasticity of the external rotators.
Figure 11-5. Magnetic resonance imaging scan of a typical type II superior labral anterior-posterior (SLAP) lesion.
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In addition, muscular strengthening exercises are used to restore strength, muscular balance, and proprioception. In most overhead athletes, we emphasize the external rotators, scapular retractors, scapular depressors, core, and legs. Additionally, scapular strengthening exercises include prone horizontal abduction, prone horizontal
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Figure 11-7. Sleeper stretch.
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Figure 11-10. Passive range of motion into internal rotation stretch.
abduction at 120 degrees with external rotation (prone full can), prone extensions at 30 degrees of abduction, and prone rowing into external rotation. Total armstrengthening exercises are performed, including arm, forearm, and wrist exercises.
Figure 11-8. Supine horizontal adduction stretch.
Figure 11-9. Supine horizontal adduction with internal rotation stretch.
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Because we think that microinstability is a contributing factor to internal impingement, the goal of rehabilitation is to enhance dynamic stabilization of the shoulder. Rhythmic stabilization exercises are performed to improve proprioception, neuromuscular control, and muscular balance (Fig. 11-11). To strengthen and enhance the neuromuscular control of the external rotators, electrical muscle stimulation (300PV, Empi, St Paul, Minn) is applied (Fig. 11-12) during exercises such as standing tubing external rotation, side-lying external rotation, prone external rotation, and other rotator cuff–strengthening exercises.
Figure 11-11. Rhythmic stabilization exercises.
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exercises are progressed to incorporate perturbations before the initiation of throwing. The perturbation drills are performed with exercise tubing at 90 degrees of abduction and with a plyometrics ball (Fig. 11-17). The goal of the perturbation drills is to improve the patient’s end range stabilization. When the patient is pain free and exhibits excellent end range stability, an interval throwing program may be implemented. The return to activity phase is focused on the initiation of an interval throwing program.54 The interval throwing program is performed every other day, three times weekly, and in conjunction with a stretching, strengthening, and plyometrics program. The interval throwing is initiated at 45 feet and the distance is gradually increased to 120 feet and occasionally to 180 feet. Throwing programs are highly individualized based on the specific athlete, season, and goals; Chapter 58 discusses interval sports programs. Once the long toss program is successfully completed, a mound throwing program is initiated. When the mound program is completed, a gradual return to competition is carried out. Figure 11-12. Neuromuscular electrical stimulation applied to the infraspinatus during tubing external rotation exercises.
In the second subacute phase, the entire shoulder complex is emphasized. The patient is placed on the thrower’s ten program (Fig. 11-13),52,53 which focuses on all the muscles involved in the act of throwing. The scapula and core exercises are performed daily; one day the exercises are performed on the table and the alternating day on a physioball (Fig. 11-14). We prefer this method because it alters the challenges onto the shoulder complex. Other scapular exercises performed during this phase include side-lying neuromuscular control drills (Fig. 11-15) and plank exercises (Fig. 11-16). Additionally, during this phase, stretching and range of motion are performed to maintain the athlete’s total motion. The next phase represents the advanced strengthening phase. During this phase, the exercise intensity, velocity, and volume are all increased to prepare the athlete for the upcoming initiation of a formal interval throwing program. The exercises performed in this phase include stretching, range of motion, thrower’s ten program, dynamic stabilization drills advanced manual resistance and reactive neuromuscular control drills are initiated. These drills include proprioceptive neuromuscular fasciculation (PNF) patterns, tubing with manual resistance, and plyometrics. The plyometrics program that we use includes one- and two-hand throws, wall drills, and Plyoball bounce-back drills. (For a detailed description of plyometric exercises, see Chapter 55.) The plyometrics drills are initiated with twohand throws first and then progress to one-hand throws. The goal of plyometrics is to increase the loads onto the shoulder and entire upper extremity progressively. Manual
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Surgical Intervention for Internal Impingement Operative management of internal impingement should only be considered after failure of nonoperative measures. When a thrower is unable to return to competition despite adequate rest and rehabilitation, surgical management may be considered. The procedure should be tailored to the athlete, because each shoulder is unique and requires individualized management. The first part of any surgical procedure on the thrower’s shoulder is a thorough examination under anesthesia. This should include evaluation and documentation of ROM of the throwing and nonthrowing shoulders. This will give the surgeon a definitive assessment of the amount of spin back and amount of retroversion and total arc of motion. This will later guide the surgeon with regard to the need for capsular release or tightening. Diagnostic arthroscopy is then carried out through a standard posterior portal. This will allow complete access to the glenohumeral joint. The articular surfaces of the glenoid and humerus are assessed. The presence or absence of loose bodies is noted. The undersurface of the supraspinatus and infraspinatus are visualized, and the presence or absence of fraying or detachment is noted. The labrum and biceps tendon anchor are also well visualized through this portal. The anterior recess of the shoulder and subscapularis tendon are also seen. Next, an anterior portal is established under direct vision. The arthroscope is placed through this portal for better visualization of the posterior aspect of the rotator cuff, capsule, and labrum. Switching between portals, the surgeon can determine whether there is any labral detachment throughout the entire circumference of the labrum.
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1A. Diagonal pattern D2 extension: Involved hand will grip tubing handle overhead and out to the side. Pull tubing down and across your body to the opposite side of leg. During the motion, lead with your thumb. Perform _______ sets of _______ repetitions _______ daily.
1B. Diagonal pattern D2 flexion: Gripping tubing handle in hand of involved arm, begin with arm out from side 45° and palm facing backward. After turning palm forward, proceed to flex elbow and bring arm up and over involved shoulder. Turn palm down and reverse to take arm to starting position. Exercise should be performed _______ sets of _______ repetitions _______ daily.
2A. External rotation at 0° abduction: Stand with involved elbow fixed at side, elbow at 90° and involved arm across front of body. Grip tubing handle while the other end of tubing is fixed. Pull out arm, keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
2B. Internal rotation at 0° abduction: Standing with elbow at side fixed at 90° and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
If a tear in the labrum is present, the next determination is whether or not the tear should be simply débrided or repaired. Inner rim bucket-handle tears (type III SLAP) can usually be débrided back to a stable rim. If the labrum is detached from the glenoid rim, arthroscopic repair of the labrum can be carried out after adequate preparation of the bony attachment. These repairs are generally done using suture anchors implanted into the glenoid rim. It is
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Figure 11-13. The thrower’s ten exercise program. This program is designed to exercise the major muscles necessary for throwing; its goal is to be an organized and concise exercise program. Also, all exercises are specific to the thrower and designed to improve the strength, power, and endurance of the shoulder’s complex musculature. ABD, abduction.
important to place the anchors on the margin of the articular cartilage, not down the neck of the glenoid, to obtain adequate re-approximation of the labrum to the glenoid surface. The suture from the anchor is then passed beneath the detached portion of the labrum and an arthroscopic knot is tied to fix the labrum back to the glenoid firmly. Multiple anchors are generally used. Text continued on page 135
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2C. (Optional) External rotation at 90° abduction: Stand with shoulder abducted 90°. Grip tubing handle while the other end is fixed straight ahead, slightly lower than the shoulder. Keeping shoulder abducted, rotate shoulder back keeping elbow at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
2D. (Optional) Internal rotation at 90° abduction: Stand with shoulder abducted to 90°, externally rotated 90° and elbow bent to 90°. Keeping shoulder abducted, rotate shoulder forward, keeping elbow bent at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
3. Shoulder abduction to 90°: Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90° (shoulder level). Perform _______ sets of _______ repetitions _______ times daily.
4. Scaption, external rotation: Stand with elbow straight and thumb up. Raise arm to shoulder level at 30° angle in front of body. Do not go above shoulder height. Perform _______ sets of _______ repetitions _______ times daily.
5. Sidelying external rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90°. Keeping the elbow of involved arm fixed to side, raise arm and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
Figure 11-13 cont’d.
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6A. Prone horizontal abduction (neutral): Lie on table, face down, with involved arm hanging straight to the floor, and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6B. Prone horizontal abduction (full ER, 100° ABD): Lie on table face down, with involved arm hanging straight to the floor, and thumb rotated up (hitchhiker). Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6C. Prone rowing: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for 2 seconds, then slowly lower. Perform _______ sets of _______ repetitions _______ times daily.
6D. Prone rowing into external rotation: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause one second. Then rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90°. Hold at the top for 2 seconds, then slowly lower taking 2-3 seconds. Perform _______ sets of _______ repetitions _______ times daily.
7. Press-ups: Seated on a chair or table, place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Hold the elevated position for 2 seconds and lower body slowly. Perform _______ sets of _______ repetitions _______ times daily. Figure 11-13 cont’d.
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8. Push-ups: Start in the down position with arms in a comfortable position. Place hands no more than shoulder width apart. Push up as high as possible, rolling shoulders forward after elbows are straight. Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _______ sets of _______ repetitions _______ times daily.
9A. Elbow flexion: Standing with arm against side and palm facing inward, bend elbow upward turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
9B. Elbow extension (abduction): Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10A. Wrist extension: Supporting the forearm and with palm facing downward, raise weight in hand as far as possible. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10B. Wrist flexion: Supporting the forearm and with palm facing upward, lower a weight in hand as far as possible and then curl it up as high as possible. Hold for 2 seconds and lower slowly. Figure 11-13 cont’d.
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10C. Supination: Forearm supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm up. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
10D. Pronation: Forearm should be supported on a table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm down. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily. Figure 11-13 cont’d.
Undersurface rotator cuff pathology can be addressed through the same two working portals. Simple fraying of the undersurface of the supraspinatus or infraspinatus can be débrided using a shaver. Partial-thickness detachment from the greater tuberosity can be repaired using smallsuture transtendon anchors placed through an accessory portal or through the working portals if the area of the tear is accessible. Once the labral or rotator cuff pathology has been addressed, attention can be shifted to the capsule. Based on the clinical evaluation of the athlete and the examination under anesthesia, remembering the total arc concept, a decision can be made as to which anatomic aspect of the capsule should be addressed. If the clinical picture of rotational microinstability is present, anterior plication or thermal shrinkage can be carried out to decrease external
A
B
Figure 11-14. Prone horizontal abduction flips with a Plyoball.
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Figure 11-15. Side-lying neuromuscular control drills for the scapular. A, Scapular retraction and protraction. B, Scapular elevation and depression.
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Figure 11-16. Plank exercises for neuromuscular control of the shoulder and scapula stabilizers.
rotation and internal impingement. It is rare that a thrower requires closure of the rotator interval, because this may severely limit capsular mobility anteriorly. If it is believed that the posterior capsule is overly voluminous, plication or thermal shrinkage can be performed to decrease capsular volume.
A
If capsular plication is to be carried out, the location of plication is identified and the amount of tissue to be plicated is determined, based on the amount of tightening desired. Sutures can be passed through the capsule alone or through the labrum as well, depending on the amount of tightening desired. Again, arthroscopic passing and tying techniques are used to complete these types of procedures. If thermal shrinkage is the modality of choice, a monopolar device should be used in a linear striping pattern extending from the glenoid to the humeral head, and separated by several millimeters of unshrunk tissue. Only the areas of interest should be treated with the shrinkage probe. Careful assessment of the posterior capsule should be made before deciding whether release of the posterior capsule is indicated. A loss of internal rotation is often treated successfully with a proper stretching program for the posterior musculature. If it is necessary to perform a capsular release to improve internal rotation, although not commonly performed, this can be carefully done using an electrocautery or arthroscopic cutting device. Typically, the capsule is released from the posterior portal inferiorly toward the posterior band of the inferior glenohumeral ligament. Careful attention should be paid to remaining as close as possible to the glenoid rim to prevent injury to the nearby axillary nerve. Once the intra-articular pathology has been addressed, the arthroscope can be directed into the subacromial space through the same standard posterior portal. The dorsal side of the rotator cuff can be visualized after resection of
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B Figure 11-17. Wall dribbles using a plyometric ball (A) and incorporating end-range perturbations (B).
the subacromial bursa. If necessary, acromioplasty can also be performed through these same portals. If any rotator cuff repair has been performed, the sutures are typically tied in the subacromial space over the dorsal side of the cuff. Regardless of which surgical procedure or technique is performed, communication with the physical therapist or
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athletic trainer is of paramount importance. The rehabilitation team should be informed as to exactly what was done to the shoulder and what to expect with regard to early and long-range rehabilitation goals, such as ROM, glenohumeral translation, and any prohibited motions, modalities, and braces or restraints that may be needed. Only through direct communication will these procedures yield a high degree of success. In some cases of chronic microinstability, long-standing pathomechanics may lead to worsening injuries and subsequent severe capsular, labral, and rotator cuff pathologies. Because the capsule and glenohumeral ligaments limit and allow rotational motion in the shoulder, complete rotator cuff tearing, capsular injury, or disruption of the glenohumeral ligament(s) is a careerthreatening injury to the thrower. Repair of the thin, friable, capsular layer of the shoulder is technically difficult and, from a recovery and rehabilitation standpoint, it is difficult to regulate return of motion. Therefore, it is important to establish good habits in terms of stretching, throwing mechanics, and injury prevention for the thrower. The following section will delineate some of the intrinsic aspects of postsurgical recovery from a rehabilitation standpoint.
137
is a common cause of symptoms while the athlete is trying to progress through the rehabilitation and throwing stages of rehabilitation. Muscle training drills and exercises are performed immediately following surgery. These are done in the form of isometrics. We allow isometrics for the first 7 to 10 days in a submaximal and subpainful manner. At approximately 10 to 14 days postoperatively, a light isotonic program will be allowed. We emphasize external rotation and scapular strengthening muscles. At week 5, the athlete is allowed to progress to the full thrower’s ten program. Plyometrics is allowed at approximately 8 weeks postoperatively. These plyometrics drills are permitted using two hands and restricting the amount of external rotation. After 10 to 14 days, two-hand plyometrics drills are progressed by incorporating one-hand drills. An aggressive strengthening program is allowed, starting at week 12 and progressing to week 16. The program is adjusted according to the patient’s response to the strengthening program and response to the surgery. A gradual return to throwing is instituted at week 16.54 A return to contact sports is usually allowed at 6 to 8 months and to overhead sports by 9 to 12 months.
Following Thermal Capsular Shrinkage
POSTOPERATIVE REHABILITATION Following Capsular Plication Immediately following capsular plication surgery, we allow immediate restricted passive range of motion, but not overaggressive stretching. We do not allow excessive external rotation, elevation, or shoulder extension. Gentle passive and active-assisted range of motion are allowed during the first 2 weeks with a goal of immediate motion to stimulate proliferation of collagen tissue. At week 3, we allow internal and external rotation to be performed at 45 degrees of abduction. We allow external rotation to approximately 30 degrees. Internal rotation can be performed to touch the side. Active-assisted flexion is allowed to 90 degrees and gradually progressed past 90 degrees during week 4. At week 5, we allow internal and external rotation to be performed at 90 degrees of abduction. Our goal is to have 75 degrees of external rotation by week 6 and to have 90 degrees of external rotation at 90 degrees of abduction by week 8. Usually, by weeks 6 to 8, flexion is 170 to 180 degrees. In the case of the overhead athlete, particularly the pitcher, we want to achieve a gain of external rotation to approximately 115 degrees. This goal is usually achieved gradually, and no earlier than week 12. We do not typically stretch the athlete aggressively past 115 to 120 degrees of external rotation; rather, we let the athlete regain normal motion through functional activities within the rehabilitation program, such as plyometrics. Not restoring full external rotation in the overhead athlete
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Guidelines for rehabilitation following thermal capsular shrinkage of the shoulder are similar to those following plication, but there a few specific precautions.55,56 The rehabilitation program must be carried out cautiously during the first 4 to 6 weeks so that the athlete does not stretch excessively. Hecht and colleagues57 have demonstrated that during the first 8 weeks following a thermal procedure, the collagen tissue is extremely vulnerable to being stretched out. Thus, during the first 6 to 8 weeks, the rehabilitation specialist must be cautious about overaggressive ROM exercises. Schaefer and associates58 have demonstrated that overaggressive activities during the first 8 weeks following thermal application to patellar tendons in rabbits caused an overall increase in resting length of the tendon. Hayashi and coworkers59 have demonstrated that an inflammatory reaction is present for at least 8 weeks and may be present as long as 3 to 6 months after a thermal procedure. Often, this inflammatory reaction can lead to joint stiffness and soreness, which may limit the patient’s progression in regards to motion. Rehabilitation following a thermal capsular shrinkage must be modified and adjusted according to the patient’s response to surgery. The program needs to be assessed and adjusted weekly; not all patients appear to respond in the same manner following this surgical procedure. Another factor to consider is a concomitant procedure performed at the time of thermal capsular shrinkage.56,60 Frequently, a SLAP repair or a rotator cuff débridement is performed concomitantly with the thermal capsular shrinkage to address internal impingement.
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Following Anterior Capsular Shift Procedure An open capsular shift procedure may be another procedure performed to address shoulder instability. This requires a delicate balance between the surgical procedure and postoperative rehabilitation program. Our experience with this type of surgical procedure is to be somewhat aggressive with postoperative management. We use two rehabilitation protocols based on the goals of each patient. Most general orthopedic patients will progress cautiously to avoid overstressing their healing tissue. An accelerated rehabilitation approach based on immediate restricted motion and a gradual return to the motion is necessary for overhead athletes. During weeks 1 through 3, active-assisted ROM for ER and IR is performed with the arm in 30 degrees of abduction to patient tolerance. During weeks 2 to 4, ROM and stretching gradually progress. Active-assisted ER and IR ROM exercises are performed at 45 degrees of abduction, with the goal of 45 degrees of motion (ER and IR) by week 4. During this time, tubing exercises may be initiated for the shoulder’s internal and external rotators; rhythmic stabilization drills and co-contractions also are performed. ER-IR stretching is performed at 90 degrees of abduction at week 4 for overhead athletes and week 6 for the general orthopedic patient. At week 8, the overhead athlete should exhibit full motion (90 degrees of ER and 45 to 55 degrees of horizontal abduction) and gradually progress to full thrower’s motion between weeks 8 and 12. For general orthopedic patients, we often restore approximately 80% to 90% of their motion by week 10 and allow time and functional activities to regain their remaining motion. A return to unrestricted sports usually occurs between 6 and 9 months, depending on the patient’s sport, position, skill level, and rate of progression.
Following Superior Labral Surgery The specific rehabilitation program following surgical intervention involving the superior glenoid labrum is dependent on the severity of the pathology and type of SLAP lesion, exact surgical procedure performed (débridement versus repair), and other concomitant procedures performed because of the underlying glenohumeral joint instability that is often present. Overall, emphasis should be placed on restoring and enhancing dynamic stability of the glenohumeral joint, while at the same time ensuring that adverse stresses are not applied to healing tissue.44 Before rehabilitation, we think that it is imperative that the mechanism of injury be fully understood. For patients who sustained a SLAP lesion via a compressive injury, such as a fall on an outstretched hand, weight-bearing exercises should be avoided to minimize compression and sheer on the superior labrum. Patients with traction injuries should
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avoid heavy resisted or excessive eccentric biceps contractions. Furthermore, patients with peel-back lesions, such as overhead athletes, should avoid excessive amounts of shoulder external rotation while the SLAP lesion is healing. Thus, the mechanism of injury is an important factor to assess individually when determining appropriate rehabilitation guidelines for each patient. Although the efficacy of rehabilitation following SLAP repairs has not been documented, the following sections will provide an overview of the rehabilitation guidelines based on our clinical experience and studies on the mechanics of the glenoid labrum and pathomechanics of SLAP lesions.44,45,61-65 Débridement of Types I and III SLAP Lesions Types I and III SLAP lesions normally undergo a simple arthroscopic débridement of the frayed labrum without an anatomic repair.44 This program can be somewhat aggressive in restoring motion and function because the biceps labral anchor to the glenoid rim is stable and intact. The rate of progression during the course of postoperative rehabilitation is based on the presence and extent of concomitant lesions and patient tolerance. If, for example, significant rotator cuff fraying (partial-thickness tear) is present and treated with arthroscopic débridement, the rehabilitative program must be appropriately adapted. Generally, a sling is worn for comfort during the first 3 to 4 days following surgery. Active-assisted range of motion and passive rangeof-motion (PROM) exercises are initiated immediately following surgery, with full PROM expected within 10 to 14 days postoperatively. Flexion ROM exercises are performed to tolerance. ER and IR in the scapular plane are initiated at 45 degrees of glenohumeral abduction and advanced to 90 degrees of abduction, usually by postoperative day 4 or 5. ROM exercises may be done early because an anatomic repair has not been performed. Shoulder musculature training may begin during the first week, with the patient performing submaximal isometrics. Light isotonic strengthening for the shoulder and scapular musculature, with the exception of the biceps, is initiated during week 2. This includes ER-IR exercise tubing, sidelying ER, prone rowing, prone horizontal abduction, and prone ER. Active elevation exercises such as scapular plane elevation (full can) and lateral raises are also included. Light biceps resistance is usually not initiated until 2 weeks following surgery in an attempt to prevent débridement site irritation. Furthermore, early overaggressive elbow flexion and forearm supination exercises should be done cautiously, particularly eccentric exercises. The individual is advanced to controlled weight-training activities between postoperative weeks 4 and 6. In athletes, plyometrics exercises may be used and are initiated between weeks 4 and 5 to train the upper extremity to absorb and develop external forces. The athlete is allowed to begin a
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gradual return to sport-specific activities between postoperative weeks 7 and 10, usually with an interval sport program. The rate of return to overhead sports is often dependent on the extent of concomitant injuries. For example, an athlete with rotator cuff débridement involving 20% to 30% penetration of the rotator cuff will usually begin an interval sport program following these guidelines, whereas an athlete with more extensive pathology may need to delay initiation of the interval sport program for up to 4 months. Repair of Type II SLAP Lesions Injuries that involve detachment of the glenoid labrum– biceps complex from the glenoid rim have various causes. This type of injury may be caused by a fall, traction force, motor vehicle accident, or during sports.44 Overhead throwing athletes commonly present with a type II SLAP lesion with the biceps tendon detached from the glenoid rim. Frequently, a peel-back lesion is also present.63 The initial rehabilitative concern is to ensure that forces and loads on the repaired labrum are appropriately controlled. We think that it is important to determine the extent of the lesion and understand its exact location and number of suture anchors when devising an appropriate rehabilitation program. For example, the rate of rehabilitation progression would be slower for a SLAP repair completed with three anchors rather than one anchor, based on the extent of the pathology and tissue involvement. Postoperative rehabilitation is delayed to allow healing of the more extensive anatomic repair required to re-attach the biceps tendon anchor in a type II lesion, in comparison with types I and II lesions. The patient is instructed to sleep in a shoulder immobilizer and wear a DonJoy Ultra Sling (DonJoy, Vista, Calif) during the daytime for the first 4 weeks following surgery to protect the healing structures from excessive amounts of motion. Gradual range of motion in a protective range is performed for the first 4 weeks below 90 degrees of elevation to avoid strain on the labral repair. During the first 2 weeks, internal and external rotation ROM exercises are performed passively in the scapular plane to approximately 10 to 15 degrees of ER and 45 degrees of IR. Initial ER ROM exercises are performed cautiously to minimize strain on the labrum through the peel-back mechanism. At postoperative week 4, the patient is instructed to begin internal and external rotation ROM activities at 90 degrees of shoulder abduction, and flexion motion can be performed above 90 degrees of elevation. Motion is gradually increased to restore full range of motion (90 to 100 degrees of ER at 90 degrees of abduction) by 8 weeks and progressed to a thrower’s motion (approximately 115 to 120 degrees of ER) through week 12. Restoration of motion is usually accomplished with minimal difficulty. Isometric exercises are performed immediately postoperatively. These exercises are performed submaximally and designed to prevent shoulder atrophy. No biceps
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contractions are permitted for 8 weeks following repair. ER-IR tubing exercises are initiated at weeks 3 to 4 and progressed to include lateral raises, full can, prone rowing, and prone horizontal abduction by week 6. As the patient progresses, a full isotonic exercise program, such as the thrower’s ten program, is initiated by weeks 7 to 8. Emphasis is placed on strengthening exercises for the external rotators and scapular stabilizers. No resisted biceps activity (both elbow flexion and forearm supination) is allowed for the first 8 weeks to protect healing of the biceps anchor. Aggressive strengthening of the biceps is avoided for 12 weeks following surgery. Furthermore, weight-bearing exercises are usually not performed for at least 8 weeks to avoid compression and shearing forces on the healing labrum. Two-hand plyometrics, as well as more advanced strengthening activities, are allowed between 10 and 12 weeks, progressing to the initiation of an interval sport program at postoperative week 16. The same criteria described earlier are used to determine whether an interval sport program can be initiated. Return to play following the surgical repair of a type II SLAP lesion typically occurs at approximately 9 to 12 months following surgery.
SUMMARY Our understanding of the mechanisms and consequences of internal impingement has been greatly enhanced over the last several years. It is now accepted that internal impingement encompasses a broad spectrum of pathologies, including articular-sided partial-thickness tears of the rotator cuff, superior labral degeneration and tears, and microinstability. Examination, surgical intervention, and rehabilitation should consider each of these underlying pathologies.
References 1. Walch G, Liotard JP, Boileau P, Noel E: Postero-superior glenoid impingement. Another shoulder impingement. Rev Chir Orthop Reparatrice Appar Mot 77:571-574, 1991. 2. Neer CS 2nd: Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am. Jan 54:41-50, 1972. 3. Neer CS 2nd: Impingement lesions. Clin Orthop Relat Res (173):70-77, 1983. 4. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. 5. Jobe CM, Sidles J: Evidence for a superior glenoid impingement upon the rotator cuff. J Shoulder Elbow Surg 2:S19, 1993. 6. Halbrecht JL, Tirman P, Atkin D: Internal impingement of the shoulder: Comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy 15:253-258, 1999.
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7. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-975, 1989. 8. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 9. Kvitne RS, Jobe FW: The diagnosis and treatment of anterior instability in the throwing athlete. Clin Orthop Relat Res (291):107-123, 1993. 10. Kvitne RS, Jobe FW, Jobe CM: Shoulder instability in the overhand or throwing athlete. Clin Sports Med 14:917-935, 1995. 11. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 12. Mihata T, Lee Y, McGarry MH, et al: Excessive humeral external rotation results in increased shoulder laxity. Am J Sports Med 32:1278-1285, 2004. 13. Fitzpatrick MJ, Tibone JE, Grossman M, et al: Development of cadaveric models of a thrower’s shoulder. J Shoulder Elbow Surg 14(Suppl S):49S-57S, 2005. 14. Schneider DJ, Tibone JE, McGarry MH, et al: Biomechanical evaluation after five- and ten-millimeter anterior glenohumeral capsulorrhaphy using a novel shoulder model of increased laxity. J Shoulder Elbow Surg 14:318-323, 2005. 15. Jobe CM: Superior glenoid impingement. Current concepts. Clin Orthop Relat Res (330):98-107, 1996. 16. Davidson PA, Elattrache NS, Jobe CM, Jobe FW: Rotator cuff and posterior-superior glenoid labrum injury associated with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 4:384-390, 1995. 17. Alberta FG, Elattrache NS, Mihata T, et al: Arthroscopic anteroinferior suture plication resulting in decreased glenohumeral translation and external rotation. Study of a cadaver model. J Bone Joint Surg Am 88:179-187, 2006. 18. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. 19. Bigliani LU, Codd TP, Connor PM, et al: Shoulder motion and laxity in the professional baseball player. Am J Sports Med 25:609-613, 1997. 20. Borsa PA, Wilk KE, Jacobson JA, et al: Correlation of range of motion and glenohumeral translation in professional baseball pitchers. Am J Sports Med 33:1392-1399, 2005. 21. Borsa PA, Dover GC, Wilk KE, Reinold MM: Glenohumeral range of motion and stiffness in professional baseball pitchers. Med Sci Sports Exerc 38:21-26, 2006. 22. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. 23. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30:20-26, 2002. 24. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc 34:2052-2056, 2002. 25. Johnson L: Patterns of Shoulder Flexibility Among College Baseball Players. J Athl Train 27:44-49, 1992. 26. Meister K, Day T, Horodyski M, et al: Rotational motion changes in the glenohumeral joint of the adolescent/Little League baseball player. Am J Sports Med 33:693-698, 2005.
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27. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball pitchers. Am J Sports Med 30:347-353, 2002. 28. Reagan KM, Meister K, Horodyski MB, et al: Humeral retroversion and its relationship to glenohumeral rotation in the shoulder of college baseball players. Am J Sports Med 30:354-360, 2002. 29. Reinold MM, Wilk KE, Macrina LC, et al: Changes in shoulder and elbow passive range of motion after pitching in professional baseball players. Am J Sports Med 36:523-527, 2008. 30. Proske U, Morgan DL: Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications. J Physiol 537(Pt 2):333-345, 2001. 31. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988. 32. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med 15: 586-590, 1988. 33. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 34. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ: An electromyographic analysis of the elbow in pitching. Am J Sports Med 15:260-263, 1987. 35. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408, 1993. 36. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. 37. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR: Biomechanics of overhand throwing with implications for injuries. Sports Med 21:421-437, 1996. 38. Yanagisawa O, Niitsu M, Takahashi H, Itai Y: Magnetic resonance imaging of the rotator cuff muscles after baseball pitching. J Sports Med Phys Fitness 43:493-499, 2003. 39. Jamurtas AZ, Theocharis V, Tofas T, et al: Comparison between leg and arm eccentric exercises of the same relative intensity on indices of muscle damage. Eur J Appl Physiol 95:179-185, 2005. 40. Prasartwuth O, Taylor JL, Gandevia SC: Maximal force, voluntary activation and muscle soreness after eccentric damage to human elbow flexor muscles. J Physiol 567 (Pt 1):337-348, 2005. 41. Reisman S, Walsh LD, Proske U: Warm-up stretches reduce sensations of stiffness and soreness after eccentric exercise. Med Sci Sports Exerc 37:929-936, 2005. 42. Rizio L, Garcia J, Renard R, Got C: Anterior instability increases superior labral strain in the late cocking phase of throwing. Orthopedics 30:544-550, 2007. 43. Meister K, Buckley B, Batts J: The posterior impingement sign: Diagnosis of rotator cuff and posterior labral tears secondary to internal impingement in overhand athletes. Am J Orthop 33:412-415, 2004. 44. Wilk KE, Reinold MM, Dugas JR, et al: Current concepts in the recognition and treatment of superior labral (SLAP) lesions. J Orthop Sports Phys Ther 35:273-291, 2005. 45. Myers TH, Zemanovic JR, Andrews JR: The resisted supination external rotation test: A new test for the diagnosis of
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46.
47.
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51.
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53.
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superior labral anterior posterior lesions. Am J Sports Med 33:1315-1320, 2005. Kim SH, Ha KI, Han KY: Biceps load test: A clinical test for superior labrum anterior and posterior lesions in shoulders with recurrent anterior dislocations. Am J Sports Med 27:300-303, 1999. Kim SH, Ha KI, Ahn JH, et al: Biceps load test II: A clinical test for SLAP lesions of the shoulder. Arthroscopy 17:160164, 2001. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993. Wilk KE, Andrews JR, Arrigo CA: The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med 23:778, 1995. Bastan M, Reinold MM, Wilk KE, Crenshaw K: Scapular position in professional baseball pitchers: A three-dimension clinical measure. J Orthop Sports Phys Ther 36:A67, 2006. Macrina LC, Wilk K, Geus J, Porterfield R: The effect of pitching on scapula position on professional baseball players. J Orthop Sports Phys Ther 37:A69, 2007. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34:385-394, 2004. Reinold MM, Macrina LC, Wilk KE, et al: Electromyographic analysis of the supraspinatus and deltoid muscles during 3 common rehabilitation exercises. J Athl Train 42:464-469, 2007. Reinold MM, Wilk KE, Reed J, et al: Interval sport programs: Guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther 32:293-298, 2002. Wilk KE, Reinold MM, Dugas JR, Andrews JR: Rehabilitation following thermal-assisted capsular shrinkage of the glenohumeral joint: current concepts. J Orthop Sports Phys Ther 32:268-292, 2002.
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56. Reinold MM, Wilk KE, Hooks TR, et al: Thermal-assisted capsular shrinkage of the glenohumeral joint in overhead athletes: A 15- to 47-month follow-up. J Orthop Sports Phys Ther 33:455-467, 2003. 57. Hecht P, Hayashi K, Lu Y, et al: Monopolar radiofrequency energy effects on joint capsular tissue: potential treatment for joint instability. An in vivo mechanical, morphological, and biochemical study using an ovine model. Am J Sports Med 27:761-771, 1999. 58. Schaefer SL, Ciarelli MJ, Arnoczky SP, Ross HE: Tissue shrinkage with the holmium:yttrium aluminum garnet laser. A postoperative assessment of tissue length, stiffness, and structure. Am J Sports Med 25:841-848, 1997. 59. Hayashi K, Markel MD, Thabit G 3rd, et al: The effect of nonablative laser energy on joint capsular properties. An in vitro mechanical study using a rabbit model. Am J Sports Med 23:482-487, 1995. 60. Levitz CL, Dugas J, Andrews JR: The use of arthroscopic thermal capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy 17:573-577, 2001. 61. Andrews JR, Carson WG, Jr., McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337-341, 1985. 62. Nam EK, Snyder SJ: The diagnosis and treatment of superior labrum, anterior and posterior (SLAP) lesions. Am J Sports Med 31:798-810, 2003. 63. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 64. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 65. Burkhart SS, Morgan C: SLAP lesions in the overhead athlete. Orthop Clin North Am 32:431-441, 2001.
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CHAPTER 12 Partial Articular Supraspinatus Tendon
Avulsion (PASTA) Lesions of the Rotator Cuff Stephen J. Snyder and James L. Bond
not address significant bursal-sided fraying and fragmentation. It is paramount, then, for the surgeon to develop a thoughtful approach to PASTA lesions.
Partial-thickness rotator cuff tears (PTRCTs) are probably the most common form of rotator cuff disease. In cadaveric studies, the reported incidence of PTRCTs is between 17% and 37% of the population,1-4 with most occurring in the fifth and sixth decades of life. Before magnetic resonance imaging (MRI) and diagnostic shoulder arthroscopy, PTRCTs were difficult to recognize, much less diagnose and treat. Therefore, most scientific and clinical research has focused on full-thickness rotator cuff tears (FTRCTs). With an increase in the recognition of PTRCTs, however, there has been an increased emphasis on diagnosis, classification, and treatment.
PATHOGENESIS An understanding of the rotator cuff anatomy in normal and pathologic states is essential for the appropriate treatment of PASTA lesions. Although no study has fully elucidated one specific cause, most clinicians agree that intrinsic, extrinsic, and traumatic factors are all possible causes of PASTA tears.
PTRCTs are usually classified according to their location (articular, bursal, or complete) and arthroscopic appearance. The partial articular supraspinatus tendon avulsion (PASTA) variety of PTRCTs is significantly more common and typically more significant than its bursal-sided or intratendinous counterparts.5-11 Payne and colleagues12 have found that PASTA lesions comprise 91% of all partial-thickness tears. PASTA lesions are also more commonly associated with overhead athletes and younger patients.12-15
Intrinsic factors include changes in rotator cuff vascularity, metabolic changes associated with aging, or both. The primary vascular supply of the supraspinatus tendon is the suprascapular artery. There are lesser contributions from the subscapular artery and some osseous contributions from the circumflex arteries. The size of the vessels decreases from medial to lateral as they travel along their musculotendinous units. Interestingly, several studies have elegantly revealed that the vessels are larger and more prevalent on the bursal side of the cuff. The articular surface of the cuff is relatively hypovascular, leading many clinicians to believe that the pathology behind PASTA lesions may be associated more with a lack of vascularity rather than impingement syndrome.17,18 In support of this concept, histologic changes on the acromial undersurface of cadaveric acromions are common with bursal surface tears but not with articular surface tears.19
The natural history of PASTA lesions is not completely understood. There is little doubt, though, that this type of tendon disruption is often associated with unacceptable pain and disability and that to return the patient back to the best possible function, surgical treatment is often necessary. In a study of 40 shoulders, 28% progressed to FTRCTs in 1 year when treated nonoperatively, whereas 10% healed spontaneously.16 In another study, Fukuda and associates3 examined histologic sections of PASTA lesions and found no evidence of tissue repair. This seems to suggest that although some PASTA lesions have the potential for healing, most continue to enlarge with time.
Histologic studies have also noted that collagen is thinner and not as well organized on the articular cuff surface when compared with the corresponding layers on the bursal side of the rotator cuff.17 This lack of organization appears to correlate with a lack of strength. In a biomechanical study, Nakajima and coworkers20 have argued that the articular cuff is only one half as strong as the bursal cuff tissue. All these factors seem to contribute to and perhaps explain the clinical observation that PASTA lesions occur more often than their bursal-sided counterparts.
Operative treatment of PASTA lesions, on the other hand, presents a conundrum. There is no firm evidence that arthroscopic débridement stimulates tendon healing and patients seldom have associated impingement signs. Therefore, subacromial decompression may be of limited value. Additionally, there is usually a significant portion of healthy tendon on the bursal side that remains anatomically attached. If the surgeon chooses to incise this normal-appearing bursal cuff, she or he destroys the natural footprint. Use of the in situ transtendon technique, however, allows the bursal portion of the tendon to remain intact, but this technique is more difficult and may
In contrast to the intrinsic theories, there are some clinicians who argue for extrinsic and traumatic explanations as the primary factor in the pathogenesis of PASTA lesions. Gartsman and Milne15 have argued that coracoacromial arch narrowing can cause extrinsic impingement 143
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and differential shear stresses that affect the articular and bursal surfaces of the cuff. They noted that these shear stresses can cause a laminated disrepair on articular, bursal, and intratendinous aspects of the cuff. Trauma, on the other hand, is commonly associated with PASTA lesions. As mentioned, the repetitive microtrauma associated with the overhead athlete preferentially causes an articular surface tear.6 Several clinicians have demonstrated what has been termed by Walch and colleagues21 as internal impingement, which is slight anterior glenohumeral instability associated with articular-sided rotator cuff lesions in the overhead athlete. During the throwing motion, the anterior instability leads to articular surface tears in the absence of extrinsic impingement.22 Overhead athletes may experience posterior shoulder pain secondary to repetitive contact between the undersurface of the supraspinatus and posterosuperior glenoid during the late cocking phase of the throwing motion. Many clinicians have stated that internal impingement is exacerbated by fatigue of the dynamic stabilizers within the shoulder, coupled with excessive external rotation secondary to an overstretched anterior capsule and the repetitive pathologic microtrauma that results. There is no complete consensus about the internal impingement theory, however, some clinicians have observed PASTA lesions in an otherwise stable shoulder with no pathologic laxity. The anatomy of the rotator cuff insertion or anatomic footprint has become a widely debated topic in the recent literature; this is obviously relevant for PASTA repairs. In a study of 17 cadaveric rotator cuff footprints, Ruotolo and associates23 have noted that the supraspinatus tendon insertion is, on average, 1.7 mm from the articular margin. Additionally, studies have shown that if the cuff insertion is more than 7 mm from its articular margin insertion, the corresponding tear in the rotator cuff is greater than 50% of the supraspinatus tendon thickness.24 Knowledge of these measurements is crucial when assessing and treating PASTA lesions.
CLINICAL DIAGNOSIS Diagnosis of PASTA lesions can be difficult. Physical examination findings can be nonspecific and therefore must be correlated with imaging modalities. Lesions found on imaging studies that do not correlate with clinical findings may be insignificant. Sher and coworkers,25 in their MRI evaluation of asymptomatic individuals, have shown that not all PASTA tears are symptomatic; this further reveals our minimal understanding of the natural history of PASTA lesions. There is no doubt, however, that PASTA lesions can be a significant source of pain, particularly in the arc of motion between 60 and 120 degrees.6 Resistance to abduction
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with the shoulder positioned in 90 degrees of abduction (Jobe’s test) generally provokes pain. External rotation and abduction lag signs are uniformly negative. Weakness and positive lag tests should alert the examiner away from a PASTA lesion toward a more probable FTRCT.26 Despite the argument against external impingement as the pathologic factor behind PASTA lesions, impingement signs as described by Neer (pain with passive forward flexion) and Hawkins (pain with internal rotation of the humerus, with the arm in 90 degrees of forward flexion) are typically positive.15 Strength is commonly preserved, but pain may limit the amount of resistance that the patient can generate. Maintenance of strength in the absence of pain after subacromial injection suggests cuff inflammation, bursitis, or some type of PTRCT. In the overhead athlete, the clinician should always evaluate for subtle signs of shoulder instability, because internal impingement may be evident. There may be varying degrees of glenohumeral joint contracture with loss of internal rotation and an increase in external rotation in the dominant shoulder. Apprehension testing—external rotation force applied to the shoulder in 90 degrees of abduction and external rotation while the patient is lying in the supine position—may be positive. The relocation test, applying a posterior force to the anterior humeral head while performing the apprehension test, is a good method for eliciting subtle amounts of anterior translation of the humeral head.21 It should be noted, however, that the presence of pain without apprehension is an unreliable indicator of anterior instability and is associated with many other pathologic conditions within the shoulder. Internal impingement is commonly associated with pain at the posterior joint line, particularly with apprehension testing. Similar to the physical examination, the clinical course of patients with PASTA lesions is difficult to distinguish from that of patients with other shoulder conditions, such as impingement, biceps tendinopathy, and labral pathology. In fact, biceps tendinopathy, posterosuperior labral degeneration, or both can occur concomitantly in as many as 30% of PASTA lesions.5,21,27 Despite the difficulty in diagnosis, many patients improve with 6 months of conservative treatment
IMAGING STUDIES Because no single study is particularly accurate for the assessment of PASTA lesions, the clinician should use a wide variety of imaging modalities, such as radiography, ultrasound, arthrography, and MRI. Although radiographs are rarely helpful for the diagnosis of a PASTA lesion, they are important for evaluating any patient with shoulder pain and helpful for diagnosing acromioclavicular lesions or glenohumeral arthritis.4 The presence of changes in the
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greater tuberosity, such as notching, sclerosis, and subchondral cystic formations, may be seen in conjunction with generalized rotator cuff pathology.28 Standard x-ray views include an anteroposterior view of the shoulder, an axillary lateral view, and a supraspinatus outlet view. The supraspinatus outlet view best demonstrates a curved or hooked acromial morphology, which is seen in some individuals with PTRCTs resulting from supraspinatus outlet narrowing. An os acromiale, which can cause impingement symptoms, can be seen on an axillary lateral film. Degenerative changes of the acromioclavicular joint are seen with a 15-degree cephalic tilt anteroposterior (Zanca) view. An apical oblique (Garth) or West Point axillary view may be added if glenohumeral instability is suspected. Conventional arthrography has historically been used for the evaluation of the rotator cuff. The initial proponents touted sensitivity as high as 83% but other studies have reported arthrography to be much less valuable.6 Gartsman and Milne15 have reported that arthrography detected only 7 of 46 arthroscopically proved PASTA lesions. Walch and colleagues21 have reported positive arthrograms in only 8 of 17 surgically proved articular surface tears. As a result of these findings, other modalities have largely replaced arthrography in the detection of PASTA lesions. Ultrasound evaluation of rotator cuff integrity has proved to be a valuable tool for FTRCTs. Wiener and Seitz29 have reported a sensitivity of 94% and specificity of 93% for the diagnosis of PTRCTs, especially in patients with pacemakers. Sonography is well tolerated by the patient and is cost effective. The limitation of ultrasound, however, continues to be its reliance on experienced personnel for accurate interpretation. This operator dependence was shown by the somewhat low 41% detection rate in the study by Brenneke and Morgan.30 These limitations are particularly relevant for subtle PASTA lesions. With the development of various techniques, such as contrast arthrography, and differential arm position, such as abduction–external rotation (ABER) views, MRI improved the ability to characterize subtle cuff abnormalities. The typical pathology of a PASTA lesion on MRI is an increased signal on the articular side of the rotator cuff on T1- and T2-weighted images, consistent with a focal defect. The defect does not extend across the entirety of the tendon (Fig. 12-1). This may seem straightforward, but previous MRI reports have been disappointing in their predictive value. Gartsman and Milne15 have reported a false-negative rate of 83% in a study of arthroscopically visualized PASTA lesions. The clinical relevance is further limited by the fact that many asymptomatic individuals have abnormal rotator cuffs on MRI, especially in patients older than 40 years.25
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PASTA lesion
Figure 12-1. T2-weighted magnetic resonance imaging scan with gadolinium enhancement of a partial articular supraspinatus tendon avulsion (PASTA) tear (arrows). The lattermost aspect of the footprint of the supraspinatus is still attached.
As a result of these issues, fat suppression, positional variation, and contrast arthrography have all been used to increase diagnostic accuracy. Unfortunately, any one of these techniques used in isolation has not seemed to increase the accuracy for detecting a PASTA detection.31-33 A recent study, however, has reported accuracy as high as 91% if all these MRI methods are used.34 The ABER view is also a useful adjunct for labral lesions, which are commonly associated with PASTA lesions, especially in throwers. Regardless of recent findings, MRI findings suggestive of a PASTA lesion should be interpreted cautiously. They should be used only as an adjunct to the clinical evaluation when determining treatment options.
CLASSIFICATION A classification system of PASTA lesions as a distinct entity does not exist. Any classification system of rotator cuff pathology, however, should begin with Neer.35 This system categorized cuff abnormalities as a continuum ranging from stage I (inflammation, hemorrhage, edema) through stage II (tendon fibrosis), into stage III (tendon tearing). PTRCTs of any variety were not addressed by this classification. Therefore, Ellman36 has proposed a more detailed classification scheme that includes partial cuff tears. In this system, lesions are classified according to location (articular surface, bursal surface, or intratendinous) and depth of the tear. Grade I tears are smaller than 3 mm, grade II tears are between 3 and 6 mm, and grade III tears involve more than one half the cuff thickness (average cuff thickness, 9 to 12 mm).
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Snyder and colleagues4,27 have classified PTRCTs according to their location (articular, bursal, or complete) and arthroscopic appearance (grades 0 to 4). Grade 0 represents a normal cuff with smooth covering. Grade 1 signifies minimal superficial fraying in an area smaller than 1 cm. Grade 2 represents fraying and failure of rotator cuff fibers smaller than 2 cm. Grade 3 includes fraying and fragmentation of the whole surface of a tendon (usually the supraspinatus) smaller than 3 cm. Grade 4 lesions contain a sizable flap tear that often encompasses more than a single tendon and is larger than 3 cm. Conway37 has extended the classification of PTRCTs to include an intratendinous extension, or partial articular tears with intratendinous extension (PAINT) lesion. Extrapolating from the literature on PTRCTs, many surgeons treat PASTA lesions according to the 50% rule, because tears involving more than one half of the tendon thickness are a significant threat to cuff integrity. Thus, the presence of an Ellman or Snyder grade III PTRCT is considered an indication for surgical repair in a symptomatic patient. Clinical data, although limited, appear to support this protocol.10,13,38 It is important to note, however, that determining the cause behind the pathology of a PASTA lesion will ensure the most appropriate treatment plan.15
TREATMENT No algorithm for treatment of PASTA lesions exists. As noted, the PASTA tear may be one of several different lesions in the same shoulder. The lesion may be a red herring, especially in an active patient older than 40 years, or it may be the primary pain generator. Therefore, the treatment algorithm demands a thoughtful approach from the surgeon.
Nonoperative Treatment For most patients with a PASTA lesion, activity modification with avoidance of overhead and other activity that provokes pain should be the initial recommendation. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also help in reduction of the pain and inflammation. A physical therapy program directed toward regaining the complete shoulder range of motion should be initiated.39 Most stretches can be performed at the patient’s side to avoid the zone of impingement (60 to 120 degrees of abduction). Subacromial and/or intra-articular corticosteroid injections can also be helpful if used with great caution. No more than two injections should be given because of the potential deleterious effects on the tendons, particularly in the throwing athlete. Overhead athletes should pay particular attention on stretching out the contracted posterior capsule. Eccentric and plyometric strengthening should be included in the rehabilitation program to mimic the deceleration and
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follow-through phase of the throwing motion. Attention to a core-strengthening program is beneficial because it reduces the degree of effort that the shoulder and arm must exert during the throwing motion. Throwing mechanics must be studied and a throwing program should be instigated in regard to the new throwing motion. Finally, rehabilitation of the parascapular musculature may serve to restore normal scapulothoracic mechanics and minimize dynamic impingement secondary to scapulothoracic dyskinesis.37,40,41 Like the natural history of PASTA lesions, the success of nonoperative treatment is unknown, because there are currently no randomized prospective studies that have assessed the results of treatment with respect to patient age, tear size, location, and cause. The literature does suggest, however, that PASTA lesions frequently progress to FTRCTs. Yamanaka and Matsumoto16 have followed 40 PASTA lesions nonoperatively for 2 years and found a progression of the tear in 80% of patients. A decrease in size of the tear occurred in 10% and a disappearance of the tear occurred in the other 10%. This seems to suggest that conservative management may not be the best option.
Operative Treatment Although the effectiveness of nonoperative treatment has yet to be reported in the literature, it is generally accepted that clinical symptoms after 6 months of conservative measures is an indication to move ahead with operative intervention. Other factors, however, such as high-level athletic participation, might require earlier intervention. Various surgical techniques such as arthroscopic débridement, arthroscopic débridement with acromioplasty, rotator cuff repair with and without acromioplasty, and transtendon intra-articular rotator cuff repair with and without acromioplasty are options for the treating physician. Some surgeons may even prefer open versus mini–open repair of the PASTA lesion. Regardless of preferred technique, it is important to discuss all these options with the patient preoperatively. In our experience, arthroscopic repair provides a distinct advantage over open procedures because it allows a unique examination of the pathologic lesion and its repair while introducing minimal trauma to healthy tissues. Results of the arthroscopic débridement–only technique have been reported.42-50 Andrews, Budoff, and coworkers42,43 have reported 85% to 89% good to excellent results on overhead athletes, with follow-up of 13 to 93 months; 77% to 100% of patients had associated labral lesions and 25% had abnormalities in the long head of the biceps tendon. Whether the surgeon should combine débridement of the PASTA lesion with concomitant subacromial decompression is controversial. Few studies have examined a uniform population with similar pathologic changes. Snyder and colleagues,27 however, have retrospectively reviewed 31 patients and reported 84% good to excellent results; in this study, 13 patients did not undergo subacromial decompression
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and there was no significant difference in the outcome of this cohort of patients. Although these studies have reported good results, there is some question as to whether arthroscopic débridement alone is enough treatment for a PASTA tear. Ryu5 has reported 86% satisfactory results in the treatment of 35 PTRCTs by arthroscopic subacromial decompression but was disappointed that only 1 of the 4 patients with PASTA tears achieved a satisfactory result. These results were contrasted with those of patients who had bursal surface–only lesions. In this cohort, 94% reported a satisfactory result. In view of these results, it was suggested that articular-sided PTRCTs might achieve better results with repair rather than with débridement alone. In an effort to answer the débridement versus repair question scientifically, Weber10 has compared arthroscopic débridement and acromioplasty with arthroscopic acromioplasty and mini–open repair. The arthroscopic débridement group had 14 good and no excellent results, whereas the mini–open repair achieved 28 good and 3 excellent results. These findings seem to confirm that lesions of more than 50% of the tendon thickness in symptomatic individuals should be repaired, An accurate measurement of cuff thickness, however, has yet to be determined. Miller and Lewis13 have further studied the results of open repair; they used the thickness of the cuff tear as their primary criterion for open repair in 55 patients. In the patients with less than 50% of tendon involvement, arthroscopic subacromial decompression and cuff débridement alone was performed. In the 24 patients with more extensive tears and more than 50% involvement, the cuff was repaired by a mini–open repair or arthroscopic technique, in 20 and 4 patients, respectively. With this protocol, 95% had satisfactory results at 1-year follow-up. It was concluded that cuff repair should be carefully considered for active patients with involvement of the dominant arm and for tears extending through more than 50% of the cuff thickness. Fukuda41 has also reported on open anterior acromioplasty with repair and reported 92% satisfactory results at a longer follow-up of 34 months. Although open repair of PASTA tears has achieved good results in the literature, this technique is severely compromised by the inability to visualize the articular surface of the cuff directly. Our preferred treatment algorithm is as follows. The initial step in the treatment of a PASTA lesion is a thorough examination of the glenohumeral joint. We prefer to use the lateral decubitus position, but the beach chair modification has been used with equal success. With the arm in 15 pounds of traction and approximately 60 degrees of abduction, an excellent view of the articular cuff using a standard 30-degree arthroscope can be obtained. Hill-Sachs, labral, and other lesions that are commonly associated with PASTA tears should be carefully considered during glenohumeral arthroscopy. Matava and associates51 have reported good success with a
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dynamic assessment of a PASTA lesion, in which the arm is placed in 90 degrees of external rotation and abduction to assess the presence of impingement of the undersurface of the supraspinatus and infraspinatus against the posterosuperior cuff and labrum. Once the diagnosis of a PASTA tear is made arthroscopically, there is no reliable method to measure the thickness of the remaining bursal cuff (Fig. 12-2). Thus, the surgeon must use all the clinical information gathered in the preoperative assessment to determine the most appropriate treatment for each case. The supraspinatus outlet radiograph is important for predicting the likelihood of an impingement lesion and subsequent need for decompression surgery. MRI, especially if enhanced by gadolinium, is the best method to estimate the thickness of the tendon defect. Based on the MRI measurements, the surgeon can assess the probability of needing a complete resection versus a transtendon repair. In our practice, if 30% to 40% of the cuff tendon remains intact on the bursal side, we perform a PASTA transtendon repair. If less than 25% to 30% of good-quality bursal tendon remains, we complete the tear and repair the entire tendon as if it were a FTRCT. When we encounter a PASTA lesion, we place a marking suture on the articular surface (0 polydioxanone suture) and cover the marking suture with a Suture Saver (Linvatec, Largo, Fla) on the bursal surface (Fig. 12-3). This technique protects the marking suture during the bursectomy and allows the corresponding bursal surface to be observed easily (Fig. 12-4). When the top of the tendon is damaged in the same location on both the articular and bursal sides, it is likely that the vitality of the remaining tendon is compromised; therefore, the takedown method of cuff repair coupled with a subacromial smoothing is necessary. A blunt obturator can be inserted into the bursa in the same direction as the spinal needle to palpate
A4 RCT tear
Figure 12-2. Type A4 or partial articular supraspinatus tendon avulsion (PASTA) cuff tear. This is characterized by having a significant articular-sided flap of torn tendon. RCT, rotator cuff tear.
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Figure 12-3. Marking suture placed through the articular side of the partial articular supraspinatus tendon avulsion (PASTA) lesion.
the area of injury and evaluate the amount of viable bursal tendon. If the bursal remnant is felt to be less than 30%, the thinned area of cuff tendon is opened, using electrocautery to peel the thin leaf of tendon off the bone. A shaver and square-tipped basket punch can then trim the feathered edge (Fig. 12-5). It is important to resect enough tissue to provide a robust edge, but never remove so much that the
Figure 12-4. Illustration of how the marking suture correlates the articular-side lesion with its bursal counterpart. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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Figure 12-5. Preparation for a full-thickness cuff repair. The thin remnant of the bursal-sided cuff is peeled off the tuberosity and the feathered edge is removed.
free edge of the tendon rests medial to the articular cartilage of the humeral head. The remainder of the procedure is similar to the standard suture anchor repair of FTRCTs. We view the lesion from the lateral acromial portal (LAP) while inserting a spinal needle percutaneously next to the acromion to determine the proper position and angle for placement of a Revo anchor (Linvatec, Largo, Fla). The anchor is loaded with two strands of no. 2 Ethibond (Ethicon, Johnson & Johnson, Piscataway, NJ) suture and one strand of Herculine suture (Linvatec, Largo, Fla), with the Herculine suture between the two strands of Ethibond. The angle of insertion is approximately 45 degrees below the subchondral bone, which is critical to the success of the repair. If the angle is too vertical, the anchor will enter the softer bone of the greater tuberosity rather than the dense subchondral bone of the humeral head, risking anchor failure. Once the proper anchor placement and insertion angle are determined, a small punch is used to create a pilot hole. The anchor is then placed into the subchondral bone, ensuring that the horizontal depth guideline is seated completely below the bone and the dashed vertical guide mark is directed toward the cuff. We choose to begin passing sutures through the tendon by retrieving the posterior suture out from the anterior cannula with a crochet hook. The appropriate suture hook is then passed through the cuff from the posterior portal. The hook is passed through the cuff from top to bottom, 6 mm posterior to the anchor and 1 to 1.5 cm medial to the free edge of the tendon. A shuttle is then fed through the tendon and grasped with a clamp from the anterior canula. Once secured, the shuttle is carried out the anterior cannula and loaded with
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the posterior Ethibond suture, which is carried back through the tendon. The partner of the posterior Ethibond suture is then retrieved with the crochet hook and stored in a Suture Saver outside the posterior cannula. These steps are repeated with the middle Herculine suture. After a Suture Saver is placed around the Herculine suture pair and placed outside the posterior cannula, the anterior suture is carried out the posterior portal with the crochet hook. The proper suture hook is again introduced, but this time through the anterior cannula. The hook is passed through the cuff from top to bottom, 6 mm anterior to the anchor and approximately 1 cm medial to the cuff edge. A shuttle is pulled out the posterior cannula, loaded with the anterior Ethibond suture, and pulled back through the anterior aspect of the cuff lesion. The partner of the anterior suture is retrieved with the crochet hook and tied down to the anchor with a sliding knot and three alternating half-hitches. The scope is then transferred to the anterior portal and the Herculine sutures are pulled out through the lateral portal and tied down to the anchor. Finally, the posterior sutures are retrieved out the lateral portal and tied down to the anchor. The cuff is visualized and palpated to ensure stability and the portals are closed with a single, absorbable, subcutaneous suture. When a significant articular-sided cuff tear is present and a healthy portion of bursal tendon is intact, we prefer to repair the torn portion while leaving the bursal attachment in place. This technique is known as the PASTA repair, or transtendon technique. There are many ostensible benefits to performing this method of repair but the most significant is that the bursal portion of the tendon is left attached, thereby lessening the stress on the sutures after surgery. To qualify for a PASTA repair, there should be at least 30% of normal tendon remaining, with little or no bursal-sided cuff damage. The PASTA repair is carried out as follows. The glenohumeral diagnostic arthroscopy is performed and all frayed fragments of the torn cuff are removed. The footprint is débrided to provide a clean bony interface for tendon healing. The marking suture is passed through the center of the tear, and the scope is moved to the subacromial space. With PASTA tears, there are usually no signs of impingement and so decompression is unnecessary. If this is confirmed on bursoscopy, the scope is placed back into the glenohumeral joint and a spinal needle introduced into the joint to establish the ideal position and angle of the first Revo anchor. We begin the repair at the anterior edge of the tear. The needle is used to penetrate the cuff as close to the remaining attachment as possible. It is usually helpful to move the arm into slightly less abduction for insertion of the anchor. A smooth 5/64-cm K wire is introduced following the path chosen by the spinal needle (Fig. 12-6). The Super-Revo anchor is then placed through the bursal cuff as close to the bone attachment as possible (Fig. 12-7). The anchor is then advanced down until the horizontal
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Figure 12-6. Illustration of how the spinal needle and K wire can be used to gauge the best position for the Super-Revo anchors to enter the prepared bone. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
guideline is below the surface of the bone. The vertical hash marks are oriented so that they face the torn tendon edge if simple sutures are desired (Fig. 12-8). They are oriented perpendicularly to the edge of the tear if horizontal mattress stitches are planned. In other words, if the eyelet of the anchor is aligned parallel to the torn cuff edge
Figure 12-7. Super-Revo anchor inserted through the bursal cuff remnant and placed down to horizontal seating line. The Super-Revo anchor separates the fibers of the bursal cuff remnant but does not seem to damage it.
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edge of the flap tear (Fig. 12-9). A Shuttle Relay Suture Passer (Linvatec, Largo, Fla) is passed through the spinal needle, pulled out through the anterior cannula (Fig. 12-10), loaded with the anterior suture, carried out the lateral puncture, and clamped to its opposite tail (Fig. 12-11). This process is repeated as needed to close the tear completely.
Figure 12-8. Use of two sutures. When two sutures are used, it is helpful to color one half of each suture with a purple marker to avoid confusion.
and each limb of the suture is passed through the flap tear 8 mm apart on each side of the anchor, a mattress stitch pattern results that provides excellent juxtaposition of the torn tendon down to bone. If the simple suture technique is used, the suture that exits nearest to the torn tendon edge is retrieved out through the anterior cannula and a spinal needle is inserted 5 mm anterior to the anchor insertion and 5 mm medial to the
A
B
Figure 12-9. First green suture is retrieved out through the anterior cannula with a crochet hook.
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Figure 12-10. Simple suture technique. A, Insertion of the spinal needle through the torn portion of the cuff. A Shuttle Relay Suture Passer (Linvatec, Largo, Fla) is pushed through the spinal needle, and grasped with a clamp from the anterior portal. B, Suture passer grasped from the anterior portal. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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The arthroscope is then reintroduced into the subacromial space from the posterior portal. The sutures are located and retrieved through a crystal cannula in the lateral portal (Fig. 12-12). If the sutures slide easily, they are tied with a Samsung Medical Center (SMC) sliding-locking knot and three half-hitches. Often, however, the sutures do not slide easily and a Revo knot must be used (Fig. 12-13). After a PASTA repair, we place patients in an UltraSling (DonJoy, Vista, Calif) for 4 weeks. Because the cuff is never detached from the bone, we have not found it necessary to protect the shoulder as long as is needed for the takedown method and FTRCT repairs. The transtendon repair technique is an excellent example of the modern advantages afforded by the arthroscope. It restores the normal footprint of the rotator cuff and provides secure fixation down to bone, with minimal invasion of normal tissues (Fig. 12-14). In a study by Lo and Burkhart,52 good to excellent results were reported at minimum 1-year follow-up on all 25 patients who underwent transtendon fixation for PASTA lesions. Further studies have confirmed good results in longer follow-up (25 to 57 months); Ide and coworkers53 have reported 16 good and excellent results, with no poor results, in a cohort of 17 patients after transtendon PASTA repair.
Figure 12-12. Sutures being pulled out the lateral portal through a crystal cannula to allow knot tying. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. (In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
It appears that arthroscopic transtendon repair is a safe and effective means of PASTA repair. However, future studies still need to address the lack of randomized prospective studies with regard to PASTA lesions. Similarly, clinical outcome studies need to focus on a mechanismbased tear classification and on obtaining a more detailed
Figure 12-11. Shuttle Relay Suture Passer (Linvatec, Largo, Fla) with green suture. This is carried through the cuff to the bursal side.
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Figure 12-13. Completed repair may use various stitches. These include mattress, double-simple, and simple sutures, depending on the configuration of suture passage through the partial articular supraspinatus tendon avulsion (PASTA) tear. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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11.
12.
Super-Revo anchors
13.
Healed cuff 6 mo. after PASTA repair
14.
15. 16. Figure 12-14. Transtendon repair technique using Super-Revo anchors (arrows). This magnetic resonance imaging scan with gadolinium enhancement documents the excellent healing in this partial articular supraspinatus tendon avulsion (PASTA) lesion at 6 months postoperatively.
17.
18. 19.
natural history for PASTA tears. Perhaps the indications of operative intervention may then be more precise, providing a better evidence-based algorithm to help the surgeon know exactly when to use these exciting surgical techniques.
20.
21. References 1. Fukuda H, Craig EV, Yamanaka K, Hamada K: Partialthickness cuff tears. In Burkhead WZ Jr (ed): Rotator Cuff Disorders. Baltimore, Williams & Wilkins, 1996, pp 174-181. 2. Fukuda H, Mikasa M, Yamanaka K: Incomplete thickness rotator cuff tears diagnosed by subacromial bursography. Clin Orthop 223:51-58, 1987. 3. Fukuda H, Mikasa M, Ogawa K, et al: The color test: An intraoperative staining test for joint-side rotator cuff tearing and its extension. J Shoulder Elbow Surg 1:86-90, 1992. 4. Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ (ed): Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229. 5. Ryu RKN: Arthroscopic subacromial decompression: A clinical review. Arthroscopy 8:141-147, 1992. 6. Itoi E, Tabata S: Incomplete rotator cuff tears: Results of operative treatment. Clin Orthop 284:128-135, 1992. 7. Gartsman GM: Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg Am 72:169-180, 1990. 8. Gartsman GM: Arthroscopic treatment of rotator cuff disease. J Shoulder Elbow Surg 4:228-241, 1995. 9. Ellman H: Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop 254:64-74, 1990. 10. Weber SC: Arthroscopic debridement and acromioplasty versus mini-open repair in the management of significant
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22. 23.
24.
25.
26.
27.
28.
29.
partial-thickness tears of the rotator cuff. Orthop Clin North Am 28:79-82, 1997. Olsewski JM, Depew AD: Arthroscopic subacromial decompression and rotator cuff debridement for stage II and stage III impingement. Arthroscopy 10:61-68, 1994. Payne LZ, Altchek DW, Craig EV, Warren RF: Arthroscopic treatment of partial rotator cuff tears in young athletes: A preliminary report. Am J Sports Med 25:299-305, 1997. Miller DV, Lewis JM: Surgical management of partial rotator cuff tears. Presented at the Second Annual Meeting of the American Orthopaedic Society for Sports Medicine, Lake Buena Vista, Fla, June 1996. Andrews JR, Broussard TS, CarsonWG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. Gartsman GM, Milne JC: Articular surface partial-thickness rotator cuff tears. J Shoulder Elbow Surg 4:409-415, 1995. Yamanaka K, Matsumoto T: The joint side tear of the rotator cuff: A follow-up study by arthrography. Clin Orthop 304:68-73, 1994. Clark JM, Harryman DT II: Tendons, ligaments, and capsule of the rotator cuff: Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. Lohr JF, Uhthoff HK: The microvascular pattern of the supraspinatus tendon. Clin Orthop 254:35-38, 1990. Ozaki J, Fujimoto S, Nakagawa Y, et al: Tears of the rotator cuff of the shoulder associated with pathological changes in the acromion: A study in cadavera. J Bone Joint Surg Am 70:1224-1230, 1988. Nakajima T, Rokuuma N, Hamada K, et al: Histologic and biomechanical characteristics of the supraspinatus tendon: Reference to rotator cuff tearing. J Shoulder Elbow Surg 3:79-87, 1994. Walch G, Boileau P, Noel E, Donell ST: Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1:238-245, 1992. Jobe CM: Superior glenoid impingement. Orthop Clin North Am 28:137-143, 1997. Ruotolo C, Fow JE, Nottage WM : The supraspinatus footprint: An anatomic study of the supraspinatus insertion. Arthroscopy 20:246-249, 2004. Sakurai G, Ozaki j, Tomita Y, et al: Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus tendon: Cadaveric and clinical studies. J Shoulder Elbow Surg 7:510-515, 1998. Sher JS, Uribe JW, Posada A, et al: Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 77:10-15, 1995. Hertel R, Ballmer FT, Lambert SM, Gerber C: Lag signs in the diagnosis of rotator cuff rupture. J Shoulder Elbow Surg 5:307-313, 1996. Snyder SJ, Pachelli AF, Del Pizzo W, et al: Partial-thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1-7, 1991. Nakagawa S, Yoneda M, Hayashida K, et al: Greater tuberosity notch: An important indicator of articular-sided partial rotator cuff tears in the shoulders of throwing athletes. Am J Sports Med 29:762-770, 2001. Wiener SN, Seitz WH Jr: Sonography of the shoulder in patients with tears of the rotator cuff: Accuracy and value
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30.
31.
32.
33.
34.
35. 36. 37.
38.
39.
40.
41.
for selecting surgical options. AJR Am J Roentgenol 160:103-107, 1993. Brenneke SL, Morgan CJ: Evaluation of ultrasonogrophy as a diagnostic technique in the assessment of rotator cuff tendon tears. Am J Sports Med 20:287-289, 1992. Quinn SF, Sheley RC, Demlow TA, Szumowski J: Rotator cuff tendon tears: Evaluation with fat-suppressed MR imaging with arthroscopic correlation in 100 patients. Radiology 195:497-500, 1995. Reinus WR, Shady KL, Mirowitz SA, Totty WG: MR diagnosis of rotator cuff tears of the shoulder: Value of using T2-weighted fat-saturated images. AJR Am J Roentgenol 164:1451-1455, 1995. Hodler J, Kursunoglu-Brahme S, Snyder SJ: Rotator cuff disease: Assessment with MR arthrography versus standard MR imaging in 36 patients with arthroscopic confirmation. Radiology 182:431-436, 1992. Meister K, Thesing J, Montgomery WJ, et al: MR arthrography of partial-thickness tears of the undersurface of the rotator cuff: An arthroscopic correlation. Skeletal Radiol 33:136-141, 2004. Neer CS II: Impingement lesions. Clin Orthop 173:70-77, 1983. Ellman H: Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res 254:64-74, 1990. Conway JE: Arthroscopic repair of partial-thickness rotator cuff tears and SLAP lesions in professional baseball players. Orthop Clin North Am 32:443-456, 2001. Williams GR Jr, Iannotti JP, Rosenthal A, et al: Anatomic, histologic, and magnetic resonance imaging abnormalities of the shoulder. Clin Orthop 330:66-74, 1996. Gotoh M, Hamada K, Yamakawa H, et al: Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J Orthop Res 16:618-621, 1998. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. Fukuda H: The management of partial-thickness tears of the rotator cuff. J Bone Joint Surg Br 85:3-11, 2003.
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42. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. 43. Budoff JE, Nirschl RP, Guidi EJ: Debridement of partialthickness tears of the rotator cuff without acromioplasty: Long-term follow-up and review of the literature. J Bone Joint Surg Am 80:733-748, 1998. 44. Paulos LE, Franklin JL: Arthroscopic shoulder decompression development and application: A five-year experience. Am J Sports Med 18:180-189, 1990. 45. Wright SA, Cofield RH: Management of partial-thickness rotator cuff tears. J Shoulder Elbow Surg 5:458-466, 1996. 46. Traughber PD, Goodwin TE: Shoulder MRI: Arthroscopic correlation with emphasis on partial tears. J Comput Assist Tomogr 16:129-133, 1992. 47. Morrison DS: Conservative management of partial-thickness rotator cuff lesions. In Burkhead WZ Jr (ed): Rotator Cuff Disorders. Baltimore, Williams & Wilkins, 1996, pp 249-257. 48. Ogilvie-Harris DJ, Wiley AM: Arthroscopic surgery of the shoulder: A general appraisal. J Bone Joint Surg Br 68: 201-207, 1986. 49. Esch JC, Ozerkis LR, Helgager JA, et al: Arthroscopic subacromial decompression: Results according to the degree of rotator cuff tear. Arthroscopy 4:241-249, 1988. 50. Altchek DW, Warren RF, Wickiewicz TL, et al: Arthroscopic acromioplasty: Technique and results. J Bone Joint Surg Am 72:1198-1207, 1990. 51. Matava MJ, Purcell DB, Rudski JR: Partial-thickness rotator cuff tears. Am J Sports Med 33:1405-1417, 2005. 52. Lo IK, Burkhart SS: Transtendon arthroscopic repair of partial-thickness, articular surface tears of the rotator cuff. Arthroscopy 20:214-20, 2004. 53. Ide J, Maeda S, Takagi K: Arthroscopic transtendon repair of partial-thickness articular-side tears of the rotator cuff: Anatomical and clinical study. Am J Sports Med 33: 1672-1679, 2005. 54. McConville OR, Ianotti JP: Partial-thickness tears of the rotator cuff: Evaluation and management. J Am Acad Orthop Surg 7:32-43, 1999.
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CHAPTER 13 Calcific Tendinitis David G. Lemak and Lawrence J. Lemak
Calcific tendinitis is the diagnosis given to shoulder pain often associated with tenderness to palpation at the greater tuberosity of the humerus, subacromial impingement, or radiographic evidence of calcific deposits in the rotator cuff tendon (Fig. 13-1). It has been attributed to cell-mediated calcification and subsequent spontaneous phagocytic resorption.1 Some patients present in the active resorptive phase when acute severe pain is present. However, most cases are diagnosed incidentally or during the workup of chronic and vague shoulder pain. The primary treatment of calcific tendinitis consists of conservative management including physical therapy, antiinflammatory medications, and occasionally a subacromial injection of corticosteroid if accompanied by subacromial impingement. More aggressive treatment may include extracorporeal shock wave therapy, needling and lavage, and surgical débridement.
been attributed to patients having a more rapid diagnosis and earlier treatment with physical therapy, combined with active rest. Several causative factors have been attributed to the development of calcific tendinitis. Zones of stress, areas of increased pressure, hypoxemia, and degeneration have all been associated with this condition. Two distinct processes have been attributed to the development of calcific tendinitis—degenerative calcification and reactive calcification.6
Degenerative Calcification Many clinicians think that the rotator cuff degenerates and subsequently becomes calcific. During the fourth and fifth decades, the fascicles of the tendon undergo thinning and fibrillation. These thinned fascicles are often hypocellular and have irregular organization.6 Necrosis of the tenocytes have been associated with intracellular accumulation of calcium, often in microspheroliths of psammomas.11 These theories support Codman’s original idea that degeneration of the cuff precedes calcification.
HISTORICAL PERSPECTIVE In 1907, Painter2 described a condition associated with subdeltoid bursitis in patients with radiographic evidence of calcific deposits in the rotator cuff. Codman,3 in 1934, attributed calcification of the rotator cuff tendon to degeneration of its fibers. In 1978, Bateman4 noted that deposits of calcification arise in an area of hypovascularization and a “zone of stress” in the supraspinatus tendon. Brewer5 thought that the calcification was attributed to aging of the rotator cuff. Most recently, Uhthoff and Loehr6 have described the progressive stages of the disease ultimately associated with tendon reconstitution, a process analogous to that described by Lippmann7 in 1961.
Uhthoff6 has noted several discrepancies with this theory. First, the incidence of calcific tendinitis peaks in the fifth decade, unlike degenerative calcification, which increases with age. Similarly, degenerative diseases never exhibit a potential for self healing. Lastly, the histologic features of calcific tendinitis and degenerative calcification are different.
Reactive Calcification The process of reactive calcification has received support in the recent literature. Uhthoff6 has noted that the process of calcification is actively mediated by cells in a viable environment and has named three distinct stages in the evolution of this disease process—the precalcific, calcific, and postcalcific stages. Although these are distinct stages, they evolve in a continuum of the disease process.
PATHOGENESIS The cause of calcific tendinitis of the rotator cuff is still unknown; however, several theories have been proposed. It should be noted that it is uncommon to find this disease in patients younger than 30 years and that the process peaks in the fifth decade.6 Some investigations have shown an increased incidence in patients with diabetes mellitus,8 and women have been shown to be afflicted more often than men. There is a 10% incidence of bilateral involvement,9 and 25% of patients have concomitant rotator cuff tears.10 Most clinicians have found that the incidence of calcific tendinitis has decreased recently. This has
In the precalcific stage, the site of predilection for calcification undergoes fibrocartilaginous transformation. There is metaplasia of tenocytes into chondrocytes. Patients exhibit little or no pain during this stage of the disease.6 The next stage is known as the calcific stage. This stage is subdivided into the formative, resting, and resorptive 155
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associated with acute and often severe pain. The deposits have a thick creamy appearance that is often under pressure. Spontaneous rupture occurs most frequently into the subacromial space; however, two cases of rupture into the glenohumeral joint have been reported.6 The postcalcific phase occurs as a continuum of the resorptive phase. Here, granulation tissue containing fibroblasts and vascular channels begin to remodel the foci previously occupied by calcium. There is positive staining for type III collagen, which is subsequently replaced with type I collagen. This reconstitution phase may or may not be associated with pain.6 A
EVALUATION 5-mm Shaver
Extruded calcium deposit
B
Rotator cuff
Figure 13-1. Radiographic evidence of calcific deposits in a rotator cuff tendon. A, Arthroscopic view of supraspinatus muscle exhibiting calcific deposit extruding into subacromial space. B, Diagrammatic representation of arthroscopic view.
phases;12 Uhthoff’s formative and resorptive phases are analogous to the early and late phases of increment, respectively, originally described by Lippmann in 1961.7 The hallmark of the formative phase is the deposition of calcium crystals in the matrix vesicles. These coalesce into larger foci of calcification.13 Fibrocartilaginous septa separate the individual foci and gradually erode as the foci enlarge. The septa are generally devoid of vascular channels and inconsistently stain for type II collagen. The gross appearance of the deposits during this stage is chalklike. There may or may not be pain present during this phase.6
The diagnosis of calcific tendinitis is based on the physical examination findings and radiographic evidence of calcific deposits in the rotator cuff tendon. A routine physical examination of the shoulder should be performed. The range of motion, impingement testing, and cross-arm evaluation for acromioclavicular joint disease should be included. The motor strength of the rotator cuff should be evaluated, as well as any evidence of glenohumeral joint instability. The radiographic evaluation is of utmost importance for this diagnosis. A standard thrower’s series of radiographs for the shoulder should be evaluated. This includes anteroposterior (AP), AP internal and external, scapular Y, and axillary radiographs. Deposits within the supraspinatus can easily be viewed on the AP views (Fig. 13-2). Deposits in the infraspinatus or teres minor can be seen on the internal rotation radiograph. Those in the subscapularis are best seen on the AP external radiograph.6 Magnetic resonance imaging (MRI) is not usually indicated for the assessment of calcific tendinitis, except when the clinical findings indicate a concomitant rotator cuff tear. Although computed tomography is not routinely used, it may be beneficial in the resorptive phase when deposits can be difficult to see.
The resting phase is histologically identified by the presence of fibrocartilaginous tissue that borders the foci. The presence of this tissue indicates that the calcium deposition at that site has concluded. There may or may not be pain present during the resting phase.6 During the resorptive phase, the histologic appearance of thin-walled vascular channels occur at the periphery of foci. Subsequently, macrophages and multinucleated giant cells phagocytose the deposits. This phase is consistently
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Figure 13-2. Radiographic anteroposterior view of a right shoulder with calcific tendinitis.
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DePalma and Kruper8 have described two radiographic forms of calcific tendinitis. Type I shows a fluffy appearance of the deposits, with poorly defined margins. This is commonly seen in the resorptive phase when patients present in acute pain. Type II is characterized by discrete deposits, with well-delineated borders. These deposits are commonly seen in the subacute and chronic stages of the disease.
TREATMENT It is important to distinguish which phase of the disease process is involved when treatment options are discussed with the patient. More than 90% of patients will respond to conservative treatment and will never require more advanced therapy or surgical intervention. An effective physical therapy program to restore range of motion and a short course of anti-inflammatory mediations will often alleviate the symptoms of calcific tendinitis. If the patient presents with concomitant subacromial impingement, a corticosteroid injection into the subacromial space may also be helpful for relieving pain. There has been some evidence to support therapeutic ultrasound for the alleviation of pain associated with calcific tendinitis. A randomized double-blind study14 has shown that patients treated with ultrasound versus placebo have a greater decrease in pain and an improved quality of life after therapeutic ultrasound is used. In addition, there is a significant reduction in the radiographic size of the deposits. When patients present with pain during the resorptive phase, needling and lavage therapy is often recommended. This can be performed in the operating room or radiology suite. Two large-bore needles are used for inflow and outflow.6 Ultrasound or fluoroscopy may be used for localization of the deposits. The deposits under pressure are decompressed after localization, and copious irrigation of the subacromial space is performed. This reduction of intratendinous pressure will often alleviate pain. Extracorporeal shock wave therapy (ECSWT) has been widely used and studied in Europe with varying results. In 1999, Loew and colleagues15 randomly assigned patients to a control group, low-dose energy group, highdose energy group, and two-dose high-energy group for treatment with ECSWT. Results showed an energydependent success, with relief of pain ranging from 5% in the control group to 58% in the two-dose high-energy group. The improvements in Constant-Murley scores and radiographic dissolution of calcific foci were also noted to be dose dependent. Rompe and associates16 have compared surgical extirpation with high-energy ECSWT treatment in patients with
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chronic calcific tendinitis. It was noted that surgical treatment has superior results in patients with homogeneous deposits. However, in those with inhomogeneous deposits, ECSWT is equivalent to surgery in providing pain relief. It was concluded that ECSWT should be given priority because of its noninvasiveness. Daecke and coworkers17 have evaluated the long-term effect of ECSWT for the treatment of chronic calcific tendinitis. A prospective study of 115 patients at the 4-year follow-up found that although ECSWT has a high failure rate—20% required surgical intervention—70% of patients had success without having long-term complications. This was therefore recommended as a noninvasive treatment of calcific tendinitis of the rotator cuff.
Surgical Treatment Although conservative treatment will resolve symptoms in most patients, some will fail to improve. They continue to have progression of symptoms that affect their activities of daily living. Surgical intervention can be used in the chronic formative phase when conservative treatments have failed. Traditionally, an open deltoid-splitting approach was used via an anterior approach to the shoulder. However, advances in arthroscopic techniques will likely make this a treatment of the past. Treatment with arthroscopic surgery has several advantages. It will probably have less morbidity because of its less invasive nature, may have a better cosmetic outcome, and may offer the advantage of decreased rehabilitation time.18 Fluoroscopy or ultrasound may be needed for assistance in localization of the deposits. Once needle localization has been achieved, a longitudinal incision can be made at the level of the deposit on the bursal surface of the rotator cuff tendon. The chalky calcific deposit is removed from the subacromial space and copious lavage is performed. Any significant disruption of the tendon can be concomitantly repaired at the time of surgical débridement. This may require a side-to-side suture repair or suture anchor to the greater tuberosity. Acromioplasty should only be performed if subacromial impingement occurs in conjunction with the calcific tendinitis.19 A sling should be used for comfort, and physical therapy should be initiated immediately to achieve range of motion and prevent arthrofibrosis.
SUMMARY Calcific tendinitis is usually a self-limited disease process that is often treated successfully with conservative measures. If unsuccessful, surgical intervention may be indicated. Arthroscopic excision of the calcific deposits, with copious irrigation of the subacromial space during the chronic formative phase, is recommended for patients
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who fail conservative measures. An acromioplasty should not be performed unless concomitant subacromial impingement is present.
References 1. Uhthoff HK, Sarkar K: Calcifying tendinitis. In Rockwood CA Jr, Matsen FA III (eds): The Shoulder, vol 2. Philadelphia: WB Saunders, 1990, pp 774-790. 2. Painter C: Subdeltoid bursitis. Boston Med Surg J 156: 345-349, 1907. 3. Codman EA: The shoulder: rupture of the supraspinatus tendon and other lesions in or about the subacromial bursa. Boston, Thomas Todd, 1934, pp 178-215. 4. Bateman JE: The Shoulder and Neck. Philadelphia, WB Saunders, 1978. 5. Brewer BJ: Aging of the rotator cuff. Am J Sports Med 7:102-110, 1979. 6. Uhthoff HK, Loehr JW: Calcific tendinopathy of the rotator cuff: Pathogenesis, diagnosis, and management. J Am Acad Orthop Surg 5:183-191, 1997. 7. Lippmann RK: Observations concerning the calcific cuff deposit. Clin Orthop 20:49-60, 1961. 8. DePalma AF, Kruper JS: Long term study of shoulder joints afflicted with and treated for calcific tendinitis. Clin Orthop 20:61-72, 1961. 9. Hurt G, Baker CL: Calcific tendinitis of the shoulder. Orthop Clin North Am 34:567-575, 2003. 10. Jim YP, Hsu HC, Chang CY, et al: Coexistince of calcific tendinitis and rotator cuff tear: An arthographic study. Skeletal Radiol 22:183-185, 1993.
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11. Mohr W, Bilger S: Morphologische Grundstrukturen der Dalzifiaierten. Tendopathie and ihre Bedeutung fur die Pathogenese. Z Rheumatol 49:346-355, 1990. 12. Uhthoff HK, Sarkar K, Maynard JA: Calcifying tendinitis: A new concept of its pathogenesis. Clin Orthop 118: 164-168, 1976. 13. Sarkar K, Uhthoff HK: Ultrastructural localization of calcium in calcifying tendinitis. Arch Pathol Lab Med 102:266-269, 1978. 14. Ebenlichler GR, Erdogmus CB, Resch KL, et al: Ultrasound therapy for calcific tendinitis of the shoulder. N Engl J Med 340:1533-1538, 1999. 15. Loew M, Daecke W, Kusnierczak D, et al: Shock-wave therapy is effective for chronic calcifying tendinitis of the shoulder. J Bone Joint Surg Br 8:863-867, 1999. 16. Rompe JD, Zoellner J, Bernhard N: Shock wave therapy versus conventional surgery in the treatment of calcifying tendinitis of the shoulder. Clin Orthop Relat Res 387:72-82, 2001. 17. Daecke W, Kusnierczak D, Loew M: Long-term effects of extracorporeal shock wave therapy in chronic calcific tendinitis of the shoulder. J Shoulder Elbow Surg 11:476-480, 2002. 18. Ark JW, Flock TJ, Flatow EL, Bigliani LV: Arthroscopic treatment of calcific tendinitis of the shoulder. Arthroscopy 8:183-188, 1992. 19. Jerosch J, Strauss JM, Schmiel S: Arthroscopic treatment of calcific tendinitis of the shoulder. J Shoulder Elbow Surg 7:30-37, 1998.
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CHAPTER 14 Open Repair of the Rotator Cuff Matthew Rappé, E. Lyle Cain, Sanford S. Kunkel, Richard J. Hawkins, and James R. Andrews
sterile fashion, draping the upper extremity free. A sterile stockinette is used to drape the lower arm.
Management of a rotator cuff tear in an athlete continues to present a unique and challenging problem. The treatment for rotator cuff tears, especially in athletes, continues to evolve. Ten years ago, at our institutions, the vast majority of rotator cuff tears in athletes were fixed through an open or mini-open approach. Arthroscopic techniques and tools have vastly improved and our comfort level with these techniques has increased in the last 10 years, so the treatment algorithm has changed. We now treat most rotator cuff tears arthroscopically and reserve open repairs for contact athletes with two or more tendon tears. Although it is important to understand how to perform a standard open rotator cuff repair with detachment of the anterior deltoid through a deltopectoral approach, we seldom perform this operation for fear of late deltoid avulsion, a disastrous consequence.1-3 If deemed necessary to perform an open repair for improved security of the repair, we will perform the repair through a series of windows to preserve the deltoid attachment and function.3 For the purposes of this chapter, we will outline the mini-open approach through multiple windows, as well as the standard open approach.
Bony landmarks are outlined and a standard posterior portal is created within the soft spot. Under direct arthroscopic visualization, an anterior portal is created through the rotator cuff interval. Any intra-articular procedure, such as loose body excision, labrum débridement, or labral repair, is carried out. We then perform a standard bursoscopy, removing any bursa and, in the case of a rotator cuff tear, would proceed with a standard arthroscopic subacromial decompression. If a complete tear of the supraspinatus and infraspinatus exists in a contact athlete, we would proceed with a standard mini-open repair. Although this is discussed elsewhere in this text (see Chapter 15), we will describe this operation briefly. We create a transverse skin incision approximately 3 to 4 cm at the edge of the lateral acromion. We then perform a deltoid splitting approach in the raphe between the anterior and middle thirds of the deltoid. Next, we identify the rotator cuff tear, mobilize as necessary, and place multiple modified Mason-Allen sutures through the cuff tear (Fig. 14-1).
The treatment goals in rotator cuff surgery have not changed, even though the technology used may be different. In the athlete, the primary goal for rotator cuff repair is usually to relieve pain; the secondary goal is to improve function. In the contact athlete, the cause of a rotator cuff tear is generally secondary to an isolated trauma; this differs greatly from the cause of a tear in the competitive overhead athlete. The goal for both groups of injured athletes is to return the athlete to his or her previous level of competition.
The rotator cuff footprint is roughened and anchors are placed within the medial aspect of the footprint (Fig. 14-2). The sutures from these anchors are then brought through the cuff medially to the Mason-Allen sutures previously placed (Fig. 14-3). Standard transosseous tunnels are created using an air-driven device (Curvetek, Biomet Sports Medicine, Warsaw, Ind; Fig. 14-4). The sutures within the transosseous tunnels are tied to themselves and the medial anchor sutures are secured (Fig. 14-5). We repair the tear using two rows of repair, if possible, similar to the method used for a complete full-thickness tear of the subscapularis, but the approach is different. We leave the patient in the lateral position and carry out the procedure using a limited deltopectoral approach centered just lateral to the coracoid. We identify the tear and secure it to the tuberosity in the same fashion as for the miniopen repair described earlier. If all three tendons are involved, we will create both these incisions and repair the tear via each of these windows.
OPERATIVE PROCEDURE In all cases, a diagnostic arthroscopy is performed in conjunction with any rotator cuff surgery. At our institution, we prefer to perform this with the patient in the lateral decubitus position. An axillary roll is used, as well as a beanbag, to maintain positioning of the patient during the procedure. The operative arm is suspended using 15 pounds of arm traction. Preoperative intravenous antibiotics are administered to the patient. The procedure is carried out with general anesthesia but may be augmented with an interscalene block for postoperative pain. The shoulder, axilla, and hemithorax are prepared in the usual
An alternative to this technique involves a standard open rotator cuff repair. This involves an anterior deltopectoral incision performed with the patient in the modified beach 159
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Figure 14-1. Mini-open repair. The rotator cuff tear is identified, mobilized as necessary, and then multiple modified Mason-Allen sutures are placed through the cuff tear.
Figure 14-3. Sutures from anchors brought through cuff medially to Mason-Allen sutures previously placed.
chair position. The incision is made in line with the deltoid fibers using self-retaining retractors for exposure. Once the deltoid muscle attachment to the acromion is encountered, the anterior deltoid is detached from the acromioclavicular joint to the lateral border of the acromion using electrocautery. Classically, a suture is placed in this split to avoid further detachment. An alternate approach involves splitting the deltoid longitudinally and preserving its attachment on the acromion. If the deltoid muscle is detached, it is retracted from the anterior acromion and the rotator cuff tear is identified. The tear is then mobilized and repair is initiated as described for the mini-open repair, using medial suture anchors and lateral bone tunnels. If mobilization of the cuff tear is necessary, release of the coracohumeral ligament will aid in this endeavor.
On completion, the repair should be watertight and checked to ensure that it is secure. The repair may be performed with the patient’s arm in the abducted position secondary to excessive tension on the cuff. The point at which the cuff comes under excessive tension should be noted for postoperative positioning and rehabilitation. The repair should be performed without tension, with the arm positioned down at the side. After the wound is thoroughly irrigated, the detached deltoid muscle is re-approximated to the remaining cuff of tissue on the anterior acromion. If a secure repair cannot be achieved, the deltoid muscle can be re-approximated to the acromion using several small drill holes through the acromion and horizontal mattress sutures (Fig. 14-6).
Roughened area of bone
Figure 14-2. Rotator cuff footprint is roughened; anchors are placed within the medial aspect of the footprint.
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161
used for small to medium-sized tears without significant tension, but a large pillow and brace are used for more retracted larger tears with tension.
REHABILITATION Rehabilitation for open rotator cuff repairs is conservative in nature in comparison with mini-open and arthroscopic repairs. Rehabilitation consists of passive assisted motion until the repair is secure. After 6 to 8 weeks, active motion is again allowed. Once active motion is instituted, terminal stretching is required, but resisted motion is delayed until appropriate active motion has been achieved, usually during the third month. It is important to remind patients that rehabilitation after rotator cuff surgery takes many months; often, 6 months elapse before patients can elevate their arms above the horizontal position with comfort and efficiency4,5 (Appendix 14-1). Initial rehabilitation consists of assisted elevation and external rotation, followed by pendulum exercises, extension, and internal rotation. Active motion then begins, depending on the size of the tear and whether the repair is secure. Prolonged rehabilitation, emphasizing range-ofmotion and strengthening exercises, is continued for a minimum of 2 years. Although an open rotator cuff repair is not typically performed in overhead athletes, those who are involved in repetitive overhead sports, such as baseball pitchers, often undergo a prolonged and intense rehabilitation program for 1 to 2 years before return to the competitive arena. Throwing athletes are not permitted to
Figure 14-4. Air-driven device helps create standard transosseous tunnels.
With a mini-open deltoid splitting technique, the deltoid can be closed side to side without re-attachment to the anterior acromion. The subcutaneous layer is closed with 2-0 absorbable sutures, and the skin is re-approximated with running subcuticular 3-0 absorbable sutures. A nonadherent dressing is placed on the shoulder, and the arm is placed in a sling. A small abduction sling and pillow are
A
B
Figure 14-5. Sutures within transosseous tunnels are tied to themselves (A) and medial anchor sutures are secured (B).
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Hawkins6 have reported good results with this technique using a rotator cuff repair secured to a trough in the bone. Subacromial decompression is considered to be an important component of rotator cuff repairs, to allow space for tissue edema and healing postoperatively. Rotator cuff pathology caused by anterior instability may necessitate anterior capsulolabral reconstruction concomitant with rotator cuff repair. The goals in rotator cuff surgery are to relieve pain and then to improve function. Appropriate patient selection and meticulous surgical repair, coupled with an intense rehabilitation program, are the keys to success in open repair of the rotator cuff. Communication between the surgeon and rehabilitation team is critical.
References
Figure 14-6. Re-approximation of deltoid fascia to anterior acromion through vertical drill holes.
throw for a minimum of 6 months and are taken through a specific rehabilitation program that emphasizes mobility and strength, followed by a progressive throwing program. Preoperative consultation involving time parameters is helpful for patient cooperation and understanding. Open communication among the surgeon, physical therapist, and athletic trainer is important to plan the patient’s appropriate return to activities based on individual tear anatomy and repair strength.
SUMMARY The technique of open rotator cuff repair6-8 is well accepted for rotator cuff repair. This technique provides secure fixation of the ruptured ends of the rotator cuff with a watertight closure. Neer and colleagues9 and Kunkel and
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1. Gumina S, Di Giorgio G, Perugia D, Postacchini F: Deltoid detachment consequent to open surgical repair of massive rotator cuff tears. Int Orthop 32:81-84, 2008. 2. Sher JS, Iannotti JP, Warner JJ, et al: Surgical treatment of post-operative deltoid origin disruption. Clin Orthop Relat Res (343):93-98, 1997. 3. Hata Y, Saitoh S, Murakami N, et al: Atrophy of the deltoid muscle following rotator cuff surgery. J Bone Surg Am 86:1414-1419, 2004. 4. Hawkins RJ: The rotator cuff and biceps tendon. In Evarts CM (ed): Surgery of the Musculoskeletal System, 2nd ed. New York, Churchill Livingstone, 1990, pp 1393. 5. Hawkins RJ: Surgical management of rotator cuff tears. In Bateman JE, Welsh RP (eds): Surgery of the Shoulder. Philadelphia, BC Decker, 1984, pp 161. 6. Kunkel SS, Hawkins RJ: Rotator-cuff repair utilizing a trough in bone. Tech Orthop 3:51, 1989. 7. McLaughlin HL, Asherman EG: Lesions in the musculotendinous cuff of the shoulder: IV. Some observation based on the results of surgical repair. J Bone Joint Surg 33A:76, 1951 8. Yel M, Shankwiler JA, Noonan JE, Burkhead WZ. Am J Orthop 2001 Apr;30(4):347-52. Results of decompression and rotator cuff repair in patients 65 years old and older: 6- to 14-year follow-up. 9. Neer CS II, Flatow EL, Lech O: Tears of the rotator cuff: long term results of anterior acromioplasty and repair. Paper read at the 55th Annual Meeting of the American Academy of Orthopaedic Surgeons, Atlanta, GA, February 5, 1988.
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APPENDIX 14-1 Shoulder Conditioning and Therapy Checklist:
Phases I, II, and III
Postoperative Program: Rotator Cuff Repair Ice Days/week ______ “on” 15-20 minutes Phases I, II, and III Time/day ______ “off”
Phase III (week 10 or 12, depending on size of tear) Days/week ______ Times/day ______
60 minutes Active Motion (With Terminal Stretch)
Phase I (0-6 weeks or 8 weeks, depending on size of tear) Small: 6 weeks Large: 8 weeks Days/week ______ Times/day ______
Passive Motion
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Phase II (week 6 or 8, depending on size of tear) Days/week ______ Times/day ______
Active Motion (With Terminal Stretch)
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Sport Cord Strengthening
Sets
Reps
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Forward punch
1-2
10-15
Overhead punch press
1-2
10-15
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CHAPTER 15 Mini-Open Rotator
Cuff Repair Robert Afra, Ilya Voloshin, and Anthony Schepsis
Rotator cuff repair was described in the literature almost 100 years ago.1 Over the years, the technique for rotator cuff repair has undergone significant modifications. The major procedures addressing the rotator cuff tears are open, mini-open, and arthroscopic repairs. Although these can be viewed as three distinct techniques, we believe that they are better understood in a timeline as an evolution, from open to mini-open to an all-arthroscopic process. There are some indications for which a formal open rotator cuff repair is to be used, but we think that the mini-open technique remains a mainstay in the contemporary shoulder surgeon’s armamentarium. This would be especially true for patients in whom an all-arthroscopic technique using suture anchors would not provide adequate fixation of the rotator cuff tissue in primary or revision situations because of poor bone quality, inadequate bone stock, or large tear. The relevant anatomy, patient history, physical examination, and indications for rotator cuff repair are all important in the appropriate patient selection for surgical treatment. See elsewhere in this text for further discussion of these topics.
Advantages of Mini-Open Over Open Technique The mini-open technique has several advantages over the open technique. To perform an anterior acromioplasty in the open technique, it is necessary to detach the deltoid from the acromion. Because the deltoid muscle origin is preserved in the mini-open technique, the rehabilitation of the postoperative shoulder is less restricted—it is unnecessary to await deltoid attachment healing—and the rare and dreadful complication of postoperative deltoid detachment is avoided.3-6 Hata and colleagues7 have reported an increased incidence of postoperative deltoid atrophy after the open repair. They found that the thickness of the anterior deltoid fibers does not change significantly after surgery in the mini-open repair group, whereas it is significantly decreased in the open repair group at 6 and 12 months postoperatively (P ⬍ .05). It has been shown that a concomitant arthroscopic intra-articular glenohumeral evaluation and treatment of pathology during miniopen rotator cuff repair affect outcome.8,9
Advantages of Mini-Open Over Arthroscopic Approach
COMPARISON OF MINI-OPEN, ALL-ARTHROSCOPIC, AND OPEN ARTHROSCOPIC PROCEDURES
Major advantages of the mini-open technique over the arthroscopic approach include the ability to perform transosseous fixation, which possibly leads to better footprint restoration, and to place modified Mason-Allen sutures, which potentially leads to stronger suture gripping properties.
The meaning of the term arthroscopically assisted miniopen rotator cuff repair has become nebulous. There is no clearly defined cutoff point at which to convert an arthroscopic procedure into a mini-open repair. Yamaguchi2 has described two intermediary surgeries that lie somewhere in between an all–mini-open technique and an all-arthroscopic technique. The two intermediary surgeries simply vary in how much of the procedure is done arthroscopically. The first, arthroscopically assisted open repair, is arthroscopic subacromial decompression followed by open repair of the rotator cuff through a lateral deltoid-splitting approach. The mini-open arthroscopically assisted repair is arthroscopic subacromial decompression, release of adhesions, placement of tagging sutures, and débridement of the tendon edges, followed by a mini-open deltoid splitting approach that results in suture management and bone tendon fixation.
There are currently two generally acceptable methods to obtain cuff fixation to bone: suture anchors and transosseous tunnels. The literature must be searched carefully if any meaningful conclusions are to be drawn when comparing transosseous tunnels with suture anchors, especially because suturing techniques vary from one study to another in mini-open surgical procedures. Early suture anchors appear to have obtained less fixation strength than transosseous tunnels.10,11 With improved suture anchor designs, other studies have demonstrated that suture anchor constructs are stronger than transosseous tunnels.12-14 Interestingly, the anterior two thirds of the greater tuberosity have higher loads to failure for anchor fixation than the posterior one third (P ⬍ .01).15 Bynum 165
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and associates16 have determined that anchors placed at a standard depth level of the laser markings or with the eyelet proud have a higher cyclic load to failure than anchors placed at a deeper level. Chhabra and coworkers17 have shown in a biomechanical model that double-loaded suture anchors have a higher resistance to failure with cyclic loading than transosseous sutures (P ⫽ .009) or single-loaded suture anchors (P ⫽ .02). Based on biomechanical data, the weak link in the suture anchor fixation construct is the tendon-gripping strength of the suture material. Gerber and colleagues18 have shown that a modified Mason-Allen stitch has nearly twice the ultimate load to failure than a simple stitch. In a similar study, Gerber and associates19 have used a sheep model to show that a simple stitch fails 100% of the time by pulling out of the tissue; however, when using a modified Mason-Allen stitch, the strength of the suture material is the limiting factor. The fact that a modified Mason-Allen stitch can be used with the mini-open rotator cuff repair technique is a real advantage. Scheibel and Habermayer20 have described an all-arthroscopic cruciate stitch using suture anchors, but they offer no biomechanical evidence of its strength. However, MacGillivray and associates21 have described the Mac stitch, which is conceptually similar to the cruciate stitch, and they performed biomechanical testing. They used a sheep model to test the cyclic loading of four stitch configurations—simple, horizontal, Mac, and modified Mason-Allen. Ultimate tensile load was significantly higher (P ⬍ .05) for the massive cuff stitch (Mac; 233 ± 40 N) and the modified Mason-Allen stitch (246 ± 40 N) than for the simple stitch (72 ± 18 N) or horizontal stitch (77 ± 15 N). There was no significant difference in the ultimate load between the Mac and modified Mason-Allen stitches. The simple and horizontal stitches failed by tissue pull-out, whereas the Mac and Mason-Allen stitches failed by a mixture of suture breakage and pull-out. In addition to the soft tissue stitch, De Carli and coworkers23 have found that the suture material affects the fixation construct. They compared FiberWire (Arthrex, Naples, Fla) with Ethibond and found Ethibond to be much less resilient, making it more prone to breakage. FiberWire seems to increase the strength of metallic and bioabsorbable fixation devices under cyclic loading. Burkhart and colleagues,24 in a human cadaveric study, compared a transosseous construct with a simple suture technique and a transosseous construct with a horizontal mattress suture technique. They tested cadaveric shoulders for ultimate load to failure and found that the simple suture construct fails at an average of 189 N, whereas the horizontal mattress construct fails at an average of 136 N (P ⬍ .007). It must be noted that the suture was tied over the greater tuberosity in the simple suture construct, but was tied over a cortical bone bridge in the horizontal mattress construct. It is by analyzing the modes of failure in these studies that interesting conclusions can be reached. The suture used for
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the construct was a no. 2 braided polyethylene. The most common mode of failure in both groups was by suture breakage. The second most common mode of failure varied with the group. Although the simple suture construct group had more tendon failures (suture pulling through the cuff tissue), the horizontal mattress group had more bone failures (the bone bridge collapsed). Therefore, it follows that if a surgeon uses a newer “supersuture” and one of the cruciate-type stitches, a construct that ties the knot over a bone bridge that uses the greater tuberosity would be stronger than a construct that ties the knot over a bone bridge that uses the lateral humeral cortex. In a follow-up biomechanical study, Burkhart and associates25 have further evaluated the mode of failure in transosseous cuff repairs using cadaveric shoulders. The 15 specimens had almost an equal distribution of failure by suture pulling through the tendon substance versus failure by the transosseous sutures cutting through the bone bridge. However, when the specimens were stratified based on the location of the distal/lateral bone tunnel exit site, interesting findings were revealed. Of 7 specimens with the distal bone tunnel exit in cortical bone, 6 showed primarily cuff tissue failure. In contrast, of 9 specimens with the distal bone tunnel exit in metaphyseal bone, 6 showed primarily bone failure. Thus, the surgeon should try to use a newer supersuture with a cruciate-type stitch, tie the suture over the greater tuberosity, and have the bone tunnel exit in the cortex. Apreleva and coworkers26 have compared various fixation and suture methods in their efforts to reproduce the supraspinatus footprint. Transosseous simple sutures, transosseous mattress sutures, suture anchors with simple sutures, and suture anchors with mattress sutures were compared. The transosseous simple suture most approximated the native supraspinatus footprint by restoring 80% of the native footprint surface area. The other three methods covered less area, 67% of the native footprint. Park and colleagues27 have confirmed these findings of greater surface area contact with transosseous tunnels. Additionally, they found greater overall pressure distribution with bone tunnel constructs in comparison with suture anchors with simple or mattress stitches. To replicate the native footprint better, many surgeons use a double-row anchor fixation. In their study, Mazzocca and colleagues28 have demonstrated that a significantly greater supraspinatus footprint width is seen with a double-row technique compared with single-row repair. The size of the double-row suture anchor footprint obtained arthroscopically is believed to equal that obtained by mini-open techniques. Although a larger footprint has not been shown to result in larger loads to failure, the larger footprint arguably results in improved biologic quality of repair. Kim and associates,29 in a biomechanical model, have compared single-row with double-row fixation using suture anchors.
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They demonstrated an increase in strength and decrease in gapping with the double-row suture anchor fixation compared with the single-row repair (P ⬍ .05). They did not control for the number of sutures or suture anchors used, which likely explains the differences in their results and those of Mazzocca and coworkers.28 Presumably, like tendon repair, an increase in the number of sutures across the repair and the number of suture anchors augments the repair strength. The only conclusion that can be drawn is that the use of more sutures and more anchors results in more strength of repair fixation. An increase in footprint size has not been shown to improve healing potential; this has only been theorized. Burkhart and colleagues25 have compared the cyclic loading to failure of rotator cuff repair constructs using transosseous tunnels with constructs using suture anchors.14 Each construct used three simple sutures, either three transosseous tunnels or three suture anchors. They applied 180 N of tension cyclically until the cuff developed a 5- and 10-mm gap from the bone bed to which it was fixed. A 5-mm gap developed in the suture anchor construct at an average of 61 cycles, but developed in the transosseous construct after an average of 25 cycles. Similarly, although a 10-mm gap developed in the suture anchor construct at an average of 285 cycles, it developed in the transosseous construct after an average of 188 cycles. These results were described in two different articles; the number of sutures and cyclic loading method were similar, but the suture material used differed. The transosseous construct used no. 2 braided polyethylene; in contrast, the suture anchor construct used no. 2 braided polyester (Ethibond, Johnson & Johnson, New Brunswick, NJ).
Disadvantages of Mini-Open Over Arthroscopic Procedures It is important to keep in mind three potential drawbacks of mini-open over a fully arthroscopic technique. This will help the surgeon minimize the risks of complications and poor results. First, some studies have reported an increased incidence of stiffness, from 11% to 20%, following mini-open surgery versus a fully arthroscopic technique,30-32 It is postulated that this is secondary to damage to the deltoid muscle.33 Stiffness is even more common (36%) in patients with insulin-dependent diabetes mellitus for longer than 5 years who undergo open cuff repairs.34 This factor may be significant in that some of these patients required manipulation or release. Proponents of an arthroscopically assisted mini-open technique have argued that the stiffness can be avoided by performing the cuff releases arthroscopically during the index procedure, thus placing less stretch on the deltoid tissue.
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Second, shoulders undergoing an all-arthroscopic cuff repair technique seem to progress through rehabilitation more easily, in that there is less postoperative pain and better range of motion.31,35,36 Again, this is likely secondary to deltoid trauma, with manipulation and stretching of the muscle tissue. Third, the open and mini-open rotator cuff repairs are associated with an increased risk of infection.37,38 Herrera and colleagues37 have described a 2% incidence of infection in 360 arthroscopically assisted mini-open rotator cuff repairs. Six of seven (89%) patients had cultures grow Propionibacterium acnes. In addition to an average of two serial irrigation and débridement procedures and 6 weeks of antibiotics, four patients required revision rotator cuff repair. In the subsequent 300 cases, gloves were changed and the skin was re-prepared before transitioning to a mini-open procedure; there were no subsequent infections. However, there is a potential bias in this study. The patients who had a Propionibacterium infection all underwent a shoulder arthroscopy and, at the same sitting, subsequently underwent a mini-open rotator cuff repair. Thus, the infection might have been caused by the arthroscopic portals “affecting” the mini-open incision. The drop in the infection rate with re-preparation of the skin before converting to a mini-open surgery corroborates this theory.
MINI-OPEN SURGICAL TECHNIQUE The rotator cuff mini-open repair technique can be logically divided into five distinct steps—diagnostic arthroscopy, decompression, tissue mobilization, deltoid split, and re-creation of the footprint and fixation. We think it is important to perform a full arthroscopic examination to assess the architecture of partial or complete tears, tissue quality, bone quality, and concomitant intra-articular pathology adequately. We routinely perform a preoperative interscalene brachial plexus block. Patient positioning depends on the surgeon’s preference. The patient can be in the beach chair or lateral decubitus position. Both allow an arthroscopic or miniopen rotator cuff repair to be performed. Appropriate perioperative antibiotics are administered. Before skin preparation, local anesthetic with epinephrine is injected into the subacromial space to minimize bleeding. The skin is prepared and osseous landmarks are outlined—acromion, clavicle, acromioclavicular joint, coracoid, and scapular spine. Glenohumeral arthroscopy is then performed in the usual fashion. After the arthroscope is inserted through a standard posterior portal, an anterior portal is established in the rotator interval. If a full-thickness rotator cuff tear is
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not readily obvious, the surgeon who suspects a tear must be meticulous in evaluation of the tendon. We have made the clinical observation that if the rotator cuff rests on the biceps tendon, so that there is no space between them, there likely exists a tear. An 18-gauge spinal needle is placed percutaneously through the rotator cuff where an articular surface tear exists; alternatively, a 2-0 polydioxanone suture (PDS) suture can be passed and the needle withdrawn (Fig. 15-1). We use the technique described here to create “a room with a view” before creating the lateral portal, so that the lateral portal can be centered over the tear. The arthroscope in the posterior portal is re-directed into the subacromial space. The arthroscope trocar is placed into the subacromial space. The sheath-trocar is then pushed out the previously created anterior portal used during the diagnostic intra-articular arthroscopy. The cannulated metal handle with overriding cannula is positioned into the anterior part of the subacromial space. As the surgeon holds the sheath and cannula steady, the assistant replaces the trocar with the arthroscope and the metal cannulated handle with a 4.5-mm full-radius or incisor shaver. The advantage of this technique is that the shaver position is readily evident. The bursa in the anterior, posterior, and lateral subacromial space is sequentially débrided, always taking care to avoid injury to the cuff tissue. An acromioplasty for a type II or III acromion, as described by Izquierdo and Bigliani,39 can be addressed at this point or just before converting to a mini-open procedure. By delaying the blind placement of the lateral portal, one is allowed to position it strategically at the center of the rotator cuff tear under direct visualization.
Figure 15-1. Assessing for tears. An 18-gauge spinal needle is used to mark the location of an articular-sided cuff tear. The bursal side of the cuff is checked for a full-thickness tear.
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The advantage of performing the acromioplasty now is that it provides more subacromial space within which to work; the disadvantage is that the bone bleeds, obscuring visualization. We prefer to do acromioplasty just after the cuff has been mobilized, before making a mini-open incision. Once a tear is confirmed, a midlateral portal is obtained approximately 2 cm distal to the lateral acromial edge and in line with the center of the tear. Arthroscopic determination of the midlateral portal placed at the center of the tear is an essential step that effectively allows for the smallest possible deltoid muscle split, thereby limiting detachment and dissection.40 An 18-gauge needle can be used to localize the ideal position. An arthroscopic portal is made after a switching stick is used to penetrate laterally into the subacromial space in line with the spinal needle. A cannula, such as a 8.25-mm cannula, is passed with a cannulated metal handle over the switching stick if one plans on passing sutures through cuff tissue arthroscopically. Otherwise, a cannula is not necessary to perform the subacromial decompression. Characterization of the rotator cuff tear, as described by Klein and Burkhart,41 is essential to facilitate an appropriate approach. It is important to define the anterior and posterior extents of the tear and to determine the shape (L versus U). From the lateral portal, the shaver is used to débride the remaining overlying bursal tissue and an acromioplasty is done by the surgeon’s preferred method. The subacromial decompression plays two roles—it provides visualization and room within which to work and removes the source of external impingement. A radiofrequency device is used to obtain hemostasis and ablate tissue. A grasper is used to determine the excursion of the cuff. If mobilization is necessary, two traction sutures are passed using no. 2 nonabsorbable sutures through the cuff, anterior and posterior, by the surgeon’s preferred method. They can be passed through the cuff tissue using retrograde suture-passing instruments (e.g., suture lasso), antegrade suture-passing instruments (e.g., penetrator, bird’s beak), or antegrade needled instruments (e.g., Expressew, DePuy Mitek, Raynham, Mass). The traction sutures are stored outside the lateral cannula so that instruments can be passed via the lateral cannula unencumbered. An arthroscopic elevator is used on the bursal surface of the cuff anteriorly and posteriorly. The articular surface of the cuff is separated from the superior labrum (Fig. 15-2). The elevator should penetrate no deeper than 2 cm because of risk of injury to the suprascapular nerve.42 Typically, we stop the bursal surface release once we have visualized fatty tissue medially around the spinoglenoid notch. The cuff excursion is again checked. The release of the articular surface is limited to 1 cm or less medial to the superior glenoid. Further mobilization can be obtained by release of the rotator interval tissue. This release may be indicated for massive, contracted, immobile rotator cuff tears. Lo and Burkhart43 have popularized the term anterior interval slide.
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Capsule
Labrum
Biceps tendon
Glenoid
A
B
This release separates the supraspinatus tendon from the rotator interval tissue. As a result, the scarred coracohumeral ligament is released.44 This procedure is most easily performed using a cutting instrument or radiofrequency ablater from the lateral portal aimed at the coracoid base. If further release is necessary, a posterior interval slide is performed. This release separates the supraspinatus from the infraspinatus, resulting in an additional 2- to 2.5-cm excursion. Up to this point, an arthroscopic approach has clear advantages over an open technique because the deltoid tissue is left intact and over the mini-open technique because of visualization during tissue mobilization of the cuff, without overstretching of the deltoid. From this point, at any step along the way, one may transition from an arthroscopic technique to a mini-open procedure. Once the cuff tissue is mobilized, the decision to proceed to a mini-open technique is based on the bone quality of the greater tuberosity, ability to re-create the footprint, need for graft augmentation, and surgeon’s preference. The lateral portal is extended. Whether a transverse or longitudinal skin incision is made, the deltoid split occurs in the same spot along the muscle fibers. We prefer to make a transverse skin incision along Langer’s lines, incorporating the lateral portal (Fig. 15-3). For ease of repair, however, it is essential that the deltoid split be centered over the rotator cuff tear while the arm is in neutral rotation. This makes the following steps much less cumbersome. The dissection is carried out through the subcutaneous tissue. The tissue is elevated from the deltoid fascia in all four directions. The fascia and deltoid muscle are incised from the acromial edge distally for 3 to 4 cm. Particular attention must be paid not to extend the deltoid split beyond 5 cm, because it will put the axillary nerve at risk (Fig. 15-4).45 The fascial split is sutured with Vicryl to prevent distal propagation.
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Figure 15-2. An elevator is used to separate the labrum from the cuff for increased excursion. Do not penetrate deeper than 2 cm to avoid suprascapular nerve injury. A, The dotted line indicates the site of capsular release peripheral to the glenoid labrum. B, A blunt elevator is used to separate the capsule and rotator cuff tendons from the labrum. (Adapted from Warner JJ, Iannotti JP, Gerber C [eds]: Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 177-202.)
At this point in the procedure, the first four steps— diagnostic arthroscopy, decompression, tissue mobilization, and deltoid split—have been achieved. As noted, the acromioplasty can be performed at any stage in the operation before conversion to the mini-open technique. We typically defer this to the final steps of the arthroscopic portion of the surgery to minimize bleeding. The two remaining steps involve the method and type of fixation and the type of stitch to be used. There are currently two acceptable methods by which to obtain cuff fixation to bone: suture anchors and transosseous
Figure 15-3. Skin incision.
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A variation of this construct is to place a simple transosseous suture. A simple suture is placed into the cuff tissue; the caudad suture tail is passed through a bone tunnel, and the cephalad suture tail is then tied over the cuff to the caudad tail on the lateral aspect of the greater tuberosity. Various suture configurations can be used for maximal tissue-grasping strength: modified MasonAllen, cruciate, Bunnell, SCOI (Southern California Orthopaedic Institute), or simple. We prefer to use a modified Mason-Allen suture (Fig. 15-6).
Figure 15-4. Prevention of axillary nerve injury. To prevent risk of axillary nerve injury, a stitch at the distal aspect of the deltoid fascial split can be used to prevent further tearing of the fascia.
tunnels. There are several variations for the repair; these include a bone trough and transosseous tunnels, doublerow anchors, single-row anchors, and a single medial row of anchors and lateral trough with transosseous tunnels. We often use a medial row of anchors in addition to laterally placed transosseous tunnels with a trough (Fig. 15-5). The medial row sutures from the anchor are placed in a horizontal mattress stitch format. The lateral row fixation is performed with a modified Mason-Allen suture, with both ends passed through separate bone tunnels and tied over a bony bridge.
A rongeur is used to débride the lateral aspect of the greater tuberosity of tissue. Care is taken to avoid decorticating the bony bed. Excursion is checked to confirm that the cuff has been adequately mobilized and to determine the sites of anchor and bone tunnel placement (Fig. 15-7). The number of anchors is determined by the size of the tear. Ideally, the anchors are placed 1 cm apart. A punch is used to determine the bone quality. Depending on bone porosity, a 5.0-, 5.5-, or 6.5-mm anchor can be used; these can be of metal or bioabsorbable material. Although there is a correlation between cortical bone density and metal anchor pull-out strength (P ⬍ .01), this is not seen with bioabsorbable anchors.46 There are conflicting results when comparing bioabsorbable with metal anchors. Several studies in porcine models have demonstrated that metal anchors have twice the pull-out strength of bioabsorbable anchors, with a range of 185 to 570 N (P ⬍ .05).47,48 However, DeCarli and associates have compared the ultimate failure load of 5.0-mm bioabsorbable, 6.5-mm bioabsorbable, and metallic 5.0-mm anchors in a biomechanical study. They found similar ultimate failure loads, but the mode of failure varied. Whereas the metal anchors failed by anchor slippage, the bioabsorbable anchors underwent eyelet failure. Additionally, bioabsorbable anchors have been found to result in foreign body reactions and extensive osteolysis.49,50 While pulling on the traction sutures, a free needle with a tight radius of curvature is used to place the no. 2 suture from the anchor in a horizontal mattress fashion approximately 1.5 cm to 1.75 cm medial to the cuff edge. The sutures are left untied and are tagged.
Figure 15-5. Hybrid rotator cuff repair. This is comprised of a medial row of suture anchors and a lateral row of transosseous tunnels with a trough.
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A Concept rotator cuff repair system kit (ConMed Linvatec, Largo, Fla) is used to create the bone tunnels laterally (Fig. 15-8). The tunnels are placed approximately 1 cm apart so that there is an adequate bony bridge. Usually, three tunnels are placed. According to Caldwell and coworkers,51 the strength of fixation with the transosseous technique is directly proportional to the distance that the lateral tunnels exit in relation to the greater tuberosity tip. They recommend more than 10 mm.51 A no. 2 nonabsorbable suture, preferably one of the newer supersutures (e.g., FiberWire, Arthrex, Naples, Fla), on a tight curved free needle is used to place a modified Mason-Allen stitch
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A
B
171
C
Figure 15-6. Tissue-grasping suture configurations (modified Mason-Allen). A, Arrows indicate how to appropriately form stitch. B, Note that this limb passes anterior to the upper limb from image A. C, Note that this limb passes posterior to the lower limb from image A.
approximately 1 cm apart52; two are typically placed, anteriorly and posteriorly. The Mason-Allen suture is lateral to the previously placed horizontal mattress sutures from the suture anchor. The most anterior limb of the anterior Mason-Allen stitch is passed through the anterior tunnel. The most posterior suture limb of the posterior MasonAllen stitch is passed through the posterior tunnel. The two remaining limbs are passed through the middle bone tunnel (Fig. 15-9).
Figure 15-7. Simple stitch placed into the leading edge of cuff tissue can aid in traction. This helps the surgeon localize the site of anchor and bone tunnel placement and also is helpful when placing a complex cruciate stitch (e.g., modified Mason-Allen).
While the assistant pulls on the traction sutures, the surgeon ties the Mason-Allen sutures passed through the bone tunnels. Subsequently, the horizontal mattress sutures are tied. The wound is irrigated. Running 2-0 Vicryl is used to re-approximate the deltoid fascia; 0 Vicryl, 2-0 Vicryl, and 4-0 Monocryl sutures are used to close the subcutaneous tissue. We routinely use cryotherapy for additional pain control53 and to minimize swelling. We avoid the postoperative use of nonsteroidal anti-inflammatories, because they have been shown to be detrimental to rotator cuff healing.54
POSTOPERATIVE REHABILITATION
Figure 15-8. Concept rotator cuff repair system kit. (Courtesy of ConMed Linvatec, Largo, Fla.)
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The protocol described is based on a medium-sized tear (1 to 3 cm). Smaller or larger tears should have the rehabilitation protocol modified as appropriate. The arm is supported using a sling with an abduction pillow for 3 weeks. Pendulum exercises are initiated postoperative day 1 after surgery. The patient is encouraged to begin range-of-motion (ROM) exercises for the elbow, wrist, and cervical spine during this interval. The pace and vigor of therapy are dictated by the size of the tear and the amount of tension on the repair, as determined by the surgeon. Passive ROM exercises are started during the first week—external rotation and internal rotation motion in the scapular plane and flexion to tolerance. There is controversy as to when to start ROM
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A
B
exercises after rotator cuff repair. With the mini-open approach, we think that passive ROM exercises should be started relatively early. However formal active-assisted ROM exercises with a therapist are begun at 3 to 6 weeks, and active ROM should be delayed to 6 to 8 weeks. Active strengthening exercises are initiated at 3 months.
Results Of Mini-Open Repairs Eight studies55-62 of 339 patients were published from 1994 to 2002 with more than 2 years of follow-up after mini-open rotator cuff repair. The average follow-up was 4 years. An average of 90% of patients reported excellent or good results and an average of 94% of patients were satisfied. Posada and colleagues61 followed 60 patients for 6 years postoperatively who had a mini-open cuff repair with 7 small (less than 1 cm), 16 medium (1 to 3 cm), 19 large (3 to 5 cm), and 18 massive (more than 5 cm) tears. They compared results at 2 and 6 years and found that the improvement in outcome with the mini-open repair does not deteriorate with time. The improvements in pain, function, active forward flexion motion, and forward flexion strength that were seen at 2 years endured through the 6-year follow-up. Even when stratified by tear size, there was no diminution in outcomes for the large and massive tears. Interestingly, they found that patients who were undergoing revision surgery, even if the index procedure consisted solely of a subacromial decompression, were unsatisfied with their revision results. The positive results endured over time.
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Figure 15-9. Sutures passed through osseous tunnels and tied laterally. A, We prefer to pass the sutures through three cortical holes. B, With two sutures in place, the middle hole receives one end of each suture and the two outside holes each receive one suture end.
Although more recent articles tend to report on shorter follow-up times, many use statistical measures that were not previously reported. For example, Hersch and associates45 have reported results on mini-open rotator cuff repair with a 3-year average postoperative period in 22 patients, showing statistically significant improvement in pain and motion. They had 12 medium (1 to 3 cm), 5 large (3 to 5 cm), and 5 massive (more than 5 cm) tears. Symptoms improved in 95% of patients. There was a statistically significant improvement in pain (P ⫽ .0001); whereas 86% had constant pain preoperatively, only 9% had constant pain postoperatively. Also, 64% had no or slight pain postoperatively. There was a statistically significant improvement in active range of ROM postoperatively. Active elevation in the scapular plane improved from 130 degrees preoperatively to 164 degrees postoperatively (P ⫽ .0034). Postoperative strength was restored to 95% to 99% of that of the contralateral side. More importantly, Hersch and coworkers45 have determined several predictors of outcome: (1) a shorter duration of symptoms is significantly associated with a better outcome; (2) larger tears are associated with a worse UCLA shoulder score; (3) greater forward elevation strength is significantly associated with a better ConstantMurley outcome score; and (4) greater external rotation strength is significantly associated with a better American Shoulder and Elbow Surgeons (ASES) shoulder index. Other studies have reported on the outcomes of doublerow fixation. Fealy and colleagues63 have described followup results of patients undergoing a mini-open repair using
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double-row fixation—horizontal mattress stitch medially and a modified Mason-Allen stitch with anchor or bone tunnel laterally. The patients had 10 small (smaller than 1 cm), 35 medium (1 to 3 cm), and 30 large (3 to 5 cm) rotator cuff tears. Although this study did not address re-creation of the footprint, it was reported that 83% of patients returned to their preinjury level of activity.
Comparison Of Arthroscopic and Mini-Open Repair Results The reported results of studies using the mini-open technique are similar to those reported using an all-arthroscopic technique.31,64-70 Tears grouped according to size and compared with a mini-open technique and an allarthroscopic technique were found to have no difference in UCLA or ASES scores for tears of similar size. Kim and associates65 have reported that at 2 to 6 years of follow-up, results of mini-open and all-arthroscopic techniques are similar with respect to pain relief, improved function, and improved active ROM. It is important to point out that they attempted to perform all these procedures arthroscopically and used the mini-open technique as a bail-out procedure. As such, there is a selection bias in the cohort. In a long-term follow-up study, Weber71 has reported the outcomes of almost 300 patients who underwent a mini-open or an all-arthroscopic rotator cuff repair. The follow-up was approximately 6 years. Final outcomes, as measured by ASES, UCLA, and simple shoulder test scores, were not statistically different between the two groups. However, the mini-open group had several complications; two frozen shoulders required manipulation and three failed rotator cuff repairs required revision surgery. Buess and coworkers72 have also reported improved results with an arthroscopic technique over the open repair with respect to pain relief, functional mobility, and satisfaction. Two thirds of the procedures were performed using the mini-open technique. Despite good clinical outcomes, two studies73,74 have subsequently re-imaged or surgically evaluated the cuff and found a significant incidence of incomplete healing. Specifically, it appears that larger tears are more prone to re-tears or nonhealing. The figures cited, with all cuff tear sizes included, are no different among the all-arthroscopic, mini-open, and open repairs. Using an all-arthroscopic single-row rotator cuff repair technique, Boileau and colleagues75 have reported an incidence of 71% (46 of 65 shoulders) healed cuffs, as determined by computed tomography (CT) arthrography and magnetic resonance imaging (MRI). Liu and associates76 have reported a 66% overall intact rate as determined by arthrography following a mini-open repair. Similarly, Harryman and coworkers77 have reported that 65% of rotator cuff repairs remain intact, as determined by ultrasound following open reconstruction. Again, Gerber
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and associates78 have found 66% of their cuffs to be intact by MRI after open reconstruction for massive tears. Klepps and coworkers74 have prospectively evaluated postoperative rotator cuff integrity in patients undergoing open and mini-open rotator cuff repairs. As determined by MRI 1 year postoperatively, they found an overall re-tear rate of 31% (i.e., 69% of cuffs remained intact). There was no difference in age between those with an intact cuff and those with a re-torn cuff postoperatively in this study. However, those cuffs that became torn again tended to have larger initial tears (3.4 versus 2.4 cm), but the difference was not statistically significant (P ⫽ .10). Patients with small or medium tears (smaller than 3 cm) had a re-tear rate of 26%, whereas patients with large or massive tears (larger than 3 cm) had a re-tear rate of 38%, but this difference was not statistically different. Those whose repairs had failed still had a significant improvement in all areas assessed, regardless of the lack of structural integrity of the cuff. Although there was a statistically significant improvement in functional outcome measures comparing preoperative and postoperative function, as indicated by ASES, UCLA, and Constant-Murley scores, the difference between those with intact cuffs versus those with re-tears was not significant. In addition, although there was a statistically significant improvement in strength with forward flexion and external rotation—preoperative versus postoperative strength—the difference between those patients with intact cuffs versus those with re-tears was not significant in this study. Bishop and colleagues79 have corroborated the findings of the report by Klepps and associates.74 They found a similar incidence of cuff re-tears and similar results of statistically significant improvement in strength postoperatively in the patients undergoing arthroscopic rotator cuff repair. They compared patients with open rotator cuff repairs with those treated arthroscopically. Overall, 69% of the open repairs were intact by MRI at 1 year versus 53% of those fixed arthroscopically, but the difference was not statistically significant. These results were stratified by the size of the cuff tear. In tears smaller than 3 cm, 74% were intact in the open repairs and 84% in the arthroscopic group. In tears larger than 3 cm, 62% were intact in the open repairs and 24% in the arthroscopic group (this difference was not significant, but the exact figure was not reported). The patients with arthroscopic cuff repairs that remained intact at 1 year had significantly greater strength (P ⬍ .02) in forward flexion and external rotation in comparison with those with re-tears or failure of the cuff to heal at 1 year. Boileau and associates75 have reported that the improvement in strength is significantly higher than preoperative values when comparing patients with healed cuffs with those with unhealed cuffs (P ⫽ .01). Additionally, they identified several factors associated with a decreased healing rate. Patients younger than 65 years had a significantly improved rate of healing (P ⬍ .001); patients older than
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65 years had a 43% incidence of tendon healing. Tears extending into the infraspinatus or subscapularis had a much lower incidence of healing (P ⫽ .02). Interestingly, it was noted that as long as the tear is not retracted beyond the glenoid rim, the size of the tear from medial to lateral is not significant (P ⫽ .07). However, no association was shown among tendon healing and duration of symptoms, gender, or prior steroid injections. In contrast, Lam and coworkers80 have reported that with traditional open repairs, duration of symptoms beyond 34 months (P ⬍ .01), female gender (P ⬍ .05), and a high-anesthesia American Society of Anesthesiologists (ASA) grade is associated with a lower Constant-Murley score (P ⬍ 005).
SUMMARY Mini-open rotator cuff repair is a well-accepted technique, leading to successful results. The arthroscopic portion of the procedure entails a diagnostic arthroscopy, decompression, and tissue mobilization. Goals of the rotator cuff repair include minimizing tension on the repair, maximizing the strength of fixation, re-creating the tendon footprint, and instituting an efficacious rehabilitation protocol.
References 1. Codman E: Complete rupture of the supraspinatus tendon: Operative treatment with report of two successful cases. Boston Med Surg J 164:708-710, 1911. 2. Yamaguchi K: Transitioning to arthroscopic rotator cuff repair: The pros and cons. Instr Course Lect 52:81-92, 2003. 3. Bigliani LU, Cordasco FA, McIlveen SJ, Musso ES: Operative treatment of failed repairs of the rotator cuff. J Bone Joint Surg Am 74:1505-1515, 1992. 4. DeOrio JK, Cofield RH; Results of a second attempt at surgical repair of a failed initial rotator cuff repair. J Bone Joint Surg Am 66:563-567, 1984. 5. Neer CS 2nd, Marberry TA; On the disadvantages of radical acromionectomy. J Bone Joint Surg Am 63:416-419, 1981. 6. Neviaser R: Ruptures of the rotator cuff. Orthop Clin North Am 18:433-438, 1987. 7. Hata Y, Saitoh S, Murakami N, et al: Atrophy of the deltoid muscle following rotator cuff surgery. J Bone Joint Surg Am 86:1414-1419, 2004. 8. Miller C, Savoie FH: Glenohumeral abnormalities associated with full-thickness tears of the rotator cuff. Orthop Rev 23:159-162, 1994. 9. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 10. Carpenter JE, Fish DN, Huston LJ, Goldstein SA: Pull-out strength of five suture anchors. Arthroscopy 9:109-113, 1993. 11. Barber FA, Cawley P, Prudich JF: Suture anchor failure strength—an in vivo study. Arthroscopy 9:647-652, 1993. 12. Hecker AT, Shea M, Hayhurst JO, et al: Pull-out strength of suture anchors for rotator cuff and Bankart lesion repairs. Am J Sports Med 21:874-879, 1993.
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13. Reed SC, Glossop N, Ogilvie-Harris DJ: Full-thickness rotator cuff tears: A biomechanical comparison of suture versus bone anchor techniques. Am J Sports Med 24:46-48, 1996. 14. Burkhart SS, Diaz Pagàn JL, Wirth MA, Athanasiou KA: Cyclic loading of anchor-based rotator cuff repairs: Confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy 13:720-724, 1997. 15. Tingart MJ, Apreleva M, Lehtinen J, et al: Anchor design and bone mineral density affect the pull-out strength of suture anchors in rotator cuff repair: Which anchors are best to use in patients with low bone quality? Am J Sports Med 32:1466-1473, 2004. 16. Bynum CK, Lee S, Mahar A, et al: Failure mode of suture anchors as a function of insertion depth. Am J Sports Med 33:1030-1034, 2005. 17. Chhabra A, Goradia VK, Francke EI: In vitro analysis of rotator cuff repairs: A comparison of arthroscopically inserted tacks or anchors with open transosseous repairs. Arthroscopy 21:323-327, 2005. 18. Gerber C, Schneeberger AG, Beck M, Schlegel U: Mechanical strength of repairs of the rotator cuff. J Bone Joint Surg Br 76:371-380, 1994. 19. Gerber C, Schneeberger AG, Perren SM, Nyffeler RW: Experimental rotator cuff repair: A preliminary study. J Bone Joint Surg Am 81:1281-1290, 1999. 20. Scheibel MT, Habermeyer P: A modified Mason-Allen technique for rotator cuff repair using suture anchors. Arthroscopy 19:330-333, 2003. 21. MacGillivray, J, Ma CB: An arthroscopic stitch for massive rotator cuff tears: The Mac stitch. Arthroscopy 20:669-671, 2004. 22. Ma CB, MacGillivray JD, Clabeaux J, et al: Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am 86:1211-1216, 2004. 23. De Carli A, Vadalà A, Monaco E, et al: Effect of cyclic loading on new polyblend suture coupled with different anchors. Am J Sports Med 33:214-219, 2005. 24. Burkhart SS, Fischer SP, Nottage WM, et al: Tissue fixation security in transosseous rotator cuff repairs: A mechanical comparison of simple versus mattress sutures. Arthroscopy 12:704-708, 1996. 25. Burkhart S, Johnson TC, Wirth MA, Athanasiou KA: Cyclic loading of transosseous rotator cuff repairs: Tension overload as a possible cause of failure. Arthroscopy 13:172-176, 1997. 26. Apreleva, M, Ozbaydar M, Fitzgibbons PG, Warner JJ: Rotator cuff tears: The effect of the reconstruction method on threedimensional repair site area. Arthroscopy 18:519-526, 2002. 27. Park MC, Cadet ER, Levine WN, et al: Tendon-to-bone pressure distribution at a repaired rotator cuff footprint using transossesous suture and suture anchor fixation techniques. Am J Sports Med 33:1154-1159, 2005. 28. Mazzocca AD, Millett PJ, Guanche CA, et al: Arthroscopic single-row versus double-row suture anchor rotator cuff repair. Am J Sports Med 33:1861-1868, 2005. 29. Kim DH, Elattrache NS, Tibone JE, et al: Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med 34:407-414, 2006. 30. Williams G, Iannotti J, Luchetti W: Mini versus open repair of isolated supraspinatus tears. J Shoulder Elbow Surg 7:310, 1998.
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31. Nottage WM: A comparison of all-arthroscopic versus miniopen rotator cuff repair: Results at 45 months. Presented at the 2001 Annual Meeting of the American Academy of Orthopaedic Surgeons, San Francisco, February 2001. 32. Yamaguchi K, Ball CM, Galatz LM: Arthroscopic rotator cuff repair: Transitioning from mini-open to all-arthroscopic. Clin Orthop Relat Res 390:83-94, 2001. 33. Nicholson G: Mini-open rotator cuff repair for supraspinatus tears. Presented at the Second Biennial Shoulder and Elbow Meeting, Miami, May 2000. 34. Chen AL, Shapiro JA, Ahn AK, et al: Rotator cuff repair in patients with type 1 diabetes mellitus. J Shoulder Elbow Surg 12:416-421, 2003. 35. Weber S: Comparison of all-arthroscopic and mini-open rotator cuff repairs. Presented at the 2001 Annual Meeting of the Arthroscopy Association of North America, Seattle, February 2001. 36. Severud E, Ruotolo C, Abbott DD, Nottage WM: Allarthroscopic versus mini-open rotator cuff repair: a long term retrospective outcome comparison. Arthroscopy 19:234-238, 2003. 37. Herrera MF, Bauer G, Reynolds F, et al: Infection after miniopen rotator cuff repair. J Shoulder Elbow Surg 11:605-608, 2002. 38. Settecerri JJ, Pitner MA, Rock MG, et al: Infection after rotator cuff repair. J Shoulder Elbow Surg 8:1-5, 1999. 39. Izquierdo R, Bigliani LU: Arthroscopic acromioplasty: History, rationale, and technique. Instr Course Lect 53:13-20, 2004. 40. Snyder SJ: Evaluation and treatment of the rotator cuff. Orthop Clin North Am 24:173-192, 1993. 41. Klein JR, Burkhart SS: Identification of essential anatomic landmarks in performing arthroscopic single- and doubleinterval slides. Arthroscopy 20:765-70, 2004. 42. Warner JJ, Higgins L, Parsons IM 4th, Dowdy P: Diagnosis and treatment of anterosuperior rotator cuff tears. J Shoulder Elbow Surg 10:37-46, 2001. 43. Lo IK, Burkhart SS: Spotlight on surgical techniques. Current concepts in arthroscopic rotator cuff repair. Am J Sports Med 31:308-324, 2003. 44. Clark JM, Harryman DT 2nd: Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. 45. Hersch JC, Sgaglione NA: Arthroscopically assisted miniopen rotator cuff repairs. Functional outcome at 2- to 7-year follow-up. Am J Sports Med 28:301-311, 2000. 46. Tingart MJ, Apreleva M, Zurakowski D, Warner JJ: Pull-out strength of suture anchors used in rotator cuff repairs. J Bone Joint Surg Am 85:2190-2198, 2003. 47. Barber, FA, Herbert MA: Suture anchors: Update 1999. Arthroscopy 15:719-725. 1999. 48. Barber, FA, Herbert MA, Click JN: Internal fixation strength of suture anchors: Update 1997. Arthroscopy 13:355-362. 1997. 49. Böstman OM, Pihlajamäki HK: Adverse tissue reactions to bioabsorbable fixation devices. Clin Orthop Relat Res (371):216-227. 2000. 50. Glueck D, Wilson TC, Johnson DL: Extensive osteolysis after rotator cuff repair with a bioabsorbable suture anchor. Am J Sports Med 33:742-744, 2005. 51. Caldwell GL, Warner JP, Miller MD, et al: Strength of fixation with transosseous sutures in rotator cuff repair. J Bone Joint Surg Am 79:1064-1069, 1997.
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52. Gerber C, Schneeberger AG, Beck M, Schlegel U: Mechanical strength of repairs of the rotator cuff. J Bone Joint Surg Br 76:371-380, 1994. 53. Singh H, Osbahr DC, Holovacs TF, et al: The efficacy of continuous cryotherapy on the postoperative shoulder: A prospective, randomized investigation. J Shoulder Elbow Surg 10:522-525, 2001. 54. Cohen DB, Kawamura S, Ehteshami JR, Rodeo SA: Indomethacin and celecoxib impair rotator cuff tendon to bone healing. Am J Sports Med 34:362-369, 2006. 55. Levy HJ, Uribe JW, Delaney LG: Arthroscopic assisted rotator cuff repair: Preliminary results. Arthroscopy 6:55-60, 1990. 56. Paulos LE, Kody MH: Arthroscopically enhanced “miniapproach” to rotator cuff repair. Am J Sports Med 22:19-25, 1994. 57. Liu SH: Arthroscopically-assisted rotator cuff repair. J Bone Joint Surg Br 76:592-595, 1994. 58. Blevins FT, Warren RF, Cavo C, et al: Arthroscopic assisted rotator cuff repair: Results using a mini-open deltoid splitting approach. Arthroscopy 12:50-59, 1996. 59. Weber SC: Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy 15:126-131, 1999. 60. Park JY, Levine WN, Marra G, et al: Portal-extension approach for the repair of small and medium rotator cuff tears. Am J Sports Med 28:312-316, 2000. 61. Posada A, Uribe JW, Hechtman KS, et al: Mini-deltoid splitting rotator cuff repair: Do results deteriorate with time? Arthroscopy 16:137-141, 2000. 62. Shinners TJ, Noordsij PG, Orwin JF: Arthroscopically assisted mini-open rotator cuff repair. Arthroscopy 18:21-26, 2002. 63. Fealy S, Kingham TP, Altchek DW: Mini-open rotator cuff repair using a two-row fixation technique: Outcomes analysis in patients with small, moderate, and large rotator cuff tears. Arthroscopy 18:665-670, 2002. 64. Warner JJ, Tétreault P, Lehtinen J, Zurakowski D: Arthroscopic versus mini-open rotator cuff repair: A cohort comparison study. Arthroscopy 21:328-332, 2005. 65. Kim SH, Ha KI, Park JH, et al: Arthroscopic versus mini-open salvage repair of the rotator cuff tear: Outcome analysis at 2 to 6 years’ follow-up. Arthroscopy 19:746-754, 2003. 66. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 67. Burkhart SS: Arthroscopic repair of massive rotator cuff tears: Concept of margin convergence. Tech Shoulder Elbow Surg 1:232-239, 2000. 68. Hoffmann F, Schiller M, Reif G: Arthroscopic rotator cuff reconstruction. Orthopade 29:888-894, 2000. 69. Tauro JC: Arthroscopic rotator cuff repair: Analysis of technique and results at 2- and 3-year follow-up. Arthroscopy 14:45-51, 1998. 70. Stollsteimer GT, Savoie FH 3rd: Arthroscopic rotator cuff repair: Current indications, limitations, techniques, and results. Instr Course Lect 47:59-65, 1998. 71. Weber SS: All-arthroscopic versus mini-open rotator cuff repair: Long-term follow-up. Presented at the 2005 American Academy of Orthopaedic Surgeons Conference, Washington DC, February 2005. 72. Buess E, Steuber KU, Waibl B: Open versus arthroscopic rotator cuff repair: A comparative view of 96 cases. Arthroscopy 21:597-604, 2005.
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73. Galatz LM, Ball CM, Teefey S, et al: Complete Arthroscopic Repair of Large and Massive Rotator Cuff Tears: Correlation of Functional Outcome with Repair Integrity. Presented at the 2002 Annual Meeting of the American Academy of Orthopaedic Surgeons, Dallas, February 2002. 74. Klepps S, Bishop J, Lin J, et al: Prospective evaluation of the effect of rotator cuff integrity on the outcome of open rotator cuff repairs. Am J Sports Med 32:1716-1722, 2004. 75. Boileau P, Brassart N, Watkinson DJ, et al: Arthroscopic repair of full-thickness tears of the supraspinatus: Does the tendon really heal? J Bone Joint Surg Am 87:1229-1240, 2005. 76. Liu SH, Baker CL: Arthroscopically assisted rotator cuff repair: Correlation of functional results with integrity of the cuff. Arthroscopy 10:54-60, 1994.
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77. Harryman DT 2nd, Mack LA, Wang KY, et al: Repairs of the rotator cuff: Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am 73:982-989, 1991. 78. Gerber C, Fuchs B, Hodler J: The results of repair of massive tears of the rotator cuff. J Bone Joint Surg Am 82:505-515, 2000. 79. Bishop J: Cuff integrity following arthroscopic versus open rotator cuff repair: A prospective study. Presented at the 2004 Annual Meeting of the Arthroscopy Association of North America, Palm Springs, Fall 2004. 80. Lam F, Mok D: Open repair of massive rotator cuff tears in patients aged sixty-five years and over: Is it worthwhile? J Shoulder Elbow Surg 13:517-521, 2004.
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CHAPTER 16 Arthroscopic Rotator Cuff Repair Ammar Anbari, Nikhil N. Verma, Brian S. Cohen, and Anthony A. Romeo
With recent advances in shoulder arthroscopy, techniques for performing a successful rotator cuff repair have evolved from full open procedures to arthroscopically assisted miniopen techniques and, more recently, to all-arthroscopic techniques. Advantages of all-arthroscopic techniques include preservation of the deltoid attachment, less postoperative pain, and decreased postoperative morbidity, with earlier return of motion. However, arthroscopic repair is a technically demanding procedure that requires special instrumentation and techniques to achieve successful outcomes.
Massive, Contracted, and Immobile Tears. This pattern is more commonly seen in older patients and is exceedingly rare in young athletes. It occurs when the tendon retracts significantly. Its mobilization is impossible without performing soft tissue releases anteriorly or posteriorly, or both. Millstein and Snyder2 have introduced the SCOI (Southern California Orthopaedic Institute) rotator cuff classification. It is a descriptive classification that uses letters and numbers to describe the pathologic condition of the cuff tendon. This type of classification may be more useful for athletes because it takes into account partial tears. The location of the tear is termed A for articular-sided tears, B for bursalsided tears, and C for complete tears. For partial-thickness tears, the degree of tendon damage is given a grade between 0 and 4. Grade 0 refers to a normal cuff, with smooth covering of the synovium and bursa. Grade 1 refers to a small tear (smaller than 1 cm), with superficial bursal or synovial irritation. Grade 2 is usually smaller than 2 cm and involves actual fraying and failure of some rotator cuff fibers. Grade 3 is smaller than 3 cm, including fraying and fragmentation of tendon fibers. Grade 4 is the most severe partial cuff tear and includes a flap tear, which encompasses more than one tendon.
CLASSIFICATION With the advancement of arthroscopic techniques for rotator cuff repair has come a better understanding of tear patterns, because of the ability to visualize the tear from a number of different directions and angles. This improved visualization has led to improved classification of tear patterns (Fig. 16-1). Recognition of tear patterns is an important first step to achieving an anatomic tension-free repair. Rotator cuff tears can be classified by tear pattern, tear size, and tear location. Lo and Burkhart1 have described four main types of tears. Crescent-Shaped Tears. These tears are the simplest to repair and recognize. Tears can be large but demonstrate minimal medial retraction. Therefore, the tears can be easily mobilized laterally and secured to the greater tuberosity without excessive tension.
Complete, or C, tears are full-thickness tears and are also classified into four categories. Grade C1 is a small complete tear, such as a puncture tear. Grade C2 is a complete tear smaller than 2 cm and involving one tendon with no retraction. Grade C3 is a large complete tear involving the entire tendon and measuring 3 to 4 cm. Minimal retraction may be seen. Grade C4 is a massive rotator cuff tear, which can involve more than one tendon and is usually retracted.
U-Shaped Tears. These tears resemble crescent-shaped tears but with significant medial retraction, often to the level of the glenoid rim. Therefore, the tendon cannot be simply pulled laterally to the greater tuberosity because it will place a significant amount of tension on the repair. Special techniques such as margin convergence can be used to help mobilize these tears before repair.
Although no single classification system is universally adopted, we use a simple classification based on tendon involvement and the amount of retraction. Type I is a single-tendon tear, type II is a two-tendon tear, and type III is a three-tendon tear. Type A is a minimally displaced tendon tear. Type B is a tendon tear retracted to the humerus. Type C is a tear retracted to the glenoid. In addition, it is important to inspect the magnetic resonance imaging (MRI) scan closely to determine the degree of muscle wasting and fatty infiltration. These factors play a paramount role in predicting the outcome of a cuff repair.
L-Shaped and Reverse L-Shaped Tears. These tears initially resemble U-shaped tears. We think that U-shaped tears are L-shaped until proved otherwise. The tears involve a tendon tear from bone, with an additional longitudinal split posteriorly or, more commonly, anteriorly, resulting in the posterior leaflet retracting posteriorly and medially. Care must be taken to reduce the corners of these tears anatomically. 177
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IS
IS
SS SS
A A IS A'
RI Sub CHL
SS
IS
RI Sub
IS
RI Sub CHL
CHL SS
SS
B
RI
RI Sub IS
Sub IS
CHL SS
CHL SS
RI Sub
RI Sub IS SS
CHL
IS
CHL
SS
C Figure 16-1. Tear classification and repair strategies. These include the crescent-shaped tear (A), U-shaped tear (B), and L-shaped tear (C).
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BIOMECHANICS Several factors play a role in the success or failure of an arthroscopic rotator cuff repair. These factors include the tear pattern and size, anchor placement, suture used, and knots placed to secure the repair.
Tear Pattern and Size The larger the tear, and the more retracted it is, the less likely full function will be restored to the patient. Simple crescent and minimally retracted U-shaped tears have more successful results than larger L-shaped and massively retracted tears. We believe strongly that correct pattern identification and anatomic repair are critical to minimize stress on the repair and maximize the chance of tendon healing and functional outcome.
Anchor Placement Suture anchors are the primary choice of fixation in arthroscopic repairs. When compared with bone tunnels, suture anchors behave favorably in rotator cuff repairs. Under cyclic loading, transosseous tunnels fail at low cycles by cutting of the suture through bone. In contrast, suture anchors fail by cutting of sutures through the tendon. These failures occur at higher cycles than transosseous tunnels.3 To maximize pull-out strength, the suture anchors should be placed at a 45-degree angle to the bone, also known as dead man’s angle (Fig. 16-2).4
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Suture Type Nonabsorbable sutures are currently used for the arthroscopic treatment of rotator cuff tears. Sutures made with no. 2 Ethibond (Ethicon, Johnson & Johnson, Norwood, Mass) are strong enough for maximum physiologic loading conditions. Recently, stronger suture material such as FiberWire (Arthrex, Naples, Fla) has been introduced and incorporated into suture anchors. These no. 2 sutures are equivalent in strength to no. 5 Ethibond sutures and result in easier knot tying with less chance of suture breakage. A number of stitch configurations have been described in arthroscopic repair techniques. Most commonly, simple or mattress sutures are used. In a biomechanical comparison, Burkhart and colleagues5 have concluded that simple sutures have a 39.7% greater ultimate load compared with mattress sutures. Recently, there has been increased interest in a doublerow repair technique to improve healing rates associated with rotator cuff repair. Studies have demonstrated that double-row fixation results in an increased area of contact between the repair footprint and the greater tuberosity.5 Furthermore, biomechanical data in a cadaveric model have demonstrated that double-row fixation results in increased ultimate failure strength and decreased gap formation with cyclic loading. However, limited clinical data are available. Although increased fixation strength would seem likely to improve healing rates, it does not change the biologic issues related to poor vascularity and tissue quality. Therefore, further clinical studies are necessary to justify the increased complexity and cost associated with double-row repairs.
Knot Placement Arthroscopic knot placement has been the subject of debate for years. There are two general types of knots, sliding and nonsliding. Sliding knots such as the Duncan loop, Tennessee slider, and Revo knot require the suture to slide through the soft tissue and the anchor itself. Alternatively, nonsliding knots or half-hitch knots do not require the suture to move through the tissue or the anchor.
Figure 16-2. Anchor insertion. The anchor is inserted at a dead man’s angle with regard to the greater tuberosity to minimize the risk of anchor pull-out.
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Two factors play a role in the placement of a knot: loop security and knot security. Loop security is the ability to keep a suture loop tight while the knot is tied. Knot security refers to the effectiveness of the knot in resisting slippage when a load is applied. In a biomechanical study aimed at comparing the different sliding and nonsliding knots, Lo and associates6 have concluded that a static nonsliding knot provides the best balance of loop security and knot security. This knot is performed by placing two half-hitches in the same direction on the same post followed by three alternating half-hitches on alternating posts. If a sliding knot is chosen, it is recommended that three alternating half-hitches be placed behind it to
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improve its knot security. Moreover, the knots placed with a no. 2 FiberWire have a better knot security compared with the same knot placed with a no. 2 Ethibond suture. Therefore, for most of our applications, we use a nonsliding knot using no. 2 FiberWire.
SURGICAL INDICATIONS AND CONTRAINDICATIONS The indications for arthroscopic rotator cuff repair are similar to those established for open and mini-open repairs. The primary indications for a repair are pain followed by weakness and poor function, with a failure of conservative management. However, in young patients and athletes with symptomatic full-thickness tears, we do not believe that there is a significant role for nonoperative management. In these cases, we believe that re-establishing tendon continuity is paramount for maximizing strength and function. Furthermore, as tears become more chronic, associated muscle changes such as atrophy and fatty infiltration, as well as tear progression, may occur and lead to compromised outcomes, with subsequent surgery. Absolute contraindications include acute or chronic infections and significant medical illnesses precluding anesthesia. Relative contraindications include advanced glenohumeral arthritis or significant retraction and fatty infiltration of the tendon, along with a fixed superior migration of the humeral head.
PREOPERATIVE CONSIDERATIONS A combination of interscalene block and general anesthesia is ideal for most patients. Advantages of regional anesthesia include decreased perioperative pain and nausea. Successful results with regional anesthesia alone have been reported, although our preference is to combine it with a general anesthetic.
hypotension. In these cases, we advise lowering the back of the table down or placing the patient in a lateral decubitus position.
Patient Positioning and Draping Beach Chair Position This is our preferred position for all arthroscopic procedures with primarily subacromial pathology (Fig. 16-3). The beach chair position has a number of advantages. The anatomy is in a familiar position and is easy to reference the instruments with respect to the body and floor. This position also allows easy conversion to an open procedure. Draping The patient is aligned on the edge of the table so that the affected shoulder and scapula are exposed. We place two folded towels on the medial edge of the scapula to retract it further laterally. The back of the table is elevated completely to position the acromion parallel to the floor. The head is secured to the operating table with tape or an optional head rest may be used if the table allows it. Care should be taken to prevent excessive flexion or extension in the neck.
Examination Under Anesthesia Examination under anesthesia should be performed in all cases and is of particular importance in the athlete in whom coexisting conditions such as instability may be present. The shoulder is checked to verify normal range of motion and exclude significant stiffness or internal rotation deficit. Stability testing should be performed in anterior, posterior, and inferior directions.
Portal Placement Consistent portal placement can help surgeons achieve reproducible results (Fig. 16-4). We begin every case by outlining the bony landmarks on the skin with a marking
Maintenance of a mean arterial pressure of 70 to 90 mm Hg or a systolic pressure near 100 mm Hg allows maximal visualization and minimizes bleeding in the subacromial space. We have also used epinephrine in the arthroscopic solution to help control bleeding and maximize visualization. Obesity is a factor in both placing the portals in the correct position and in controlling blood pressure. Most surgeons tend to place portals laterally in obese patients because it may be difficult to palpate the bony landmarks. In such cases, it is advisable to use an 18-gauge spinal needle to verify the accuracy of the portals before making incisions. Moreover, an obese patient placed in the beach chair position may run the risk of developing superior vena cava compression, leading to decreased venous return to the heart and uncontrollable
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Figure 16-3. Patient positioning. The patient is placed in a beach chair position for arthroscopic rotator cuff repair.
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long head of the biceps. Although this portal can be easily established with an outside-in technique using a spinal needle, we prefer to establish it through an inside-out technique. This involves driving the arthroscope anteriorly toward the triangle and gently pushing against the anterior capsule. The arthroscope is removed and a Wissinger rod is pushed through the scope cannula to create a puncture hole in the rotator interval. The skin is tented anteriorly and a no. 11 knife blade is used to create the skin incision. Ideally, the location of the portal is just lateral to the tip of the coracoid. The rod is pushed through the skin incision and a clear cannula is placed over the rod into the joint. The Wissinger rod is withdrawn and the arthroscope is reintroduced.
Figure 16-4. Surgical landmarks placed on skin. Standard portals include posterior, direct lateral, accessory anterolateral, and anteriorsuperior portals.
pen. Some bony landmarks should be palpable in most patients. The posterior and anterior corners of the acromion, as well as the soft spot between the posterior clavicle and anterior scapular spine, should be marked first. A line is drawn between the two corners of the acromion. The anterior and posterior edges of the clavicle are marked next, along with the scapular spine. The acromioclavicular (AC) joint is palpated and marked. Finally, a circle is drawn over the prominence of the coracoid.
Lateral Portal This is the viewing portal for arthroscopic cuff repairs and for the second stage of a subacromial decompression. It is only used for subacromial work. The ideal location of this portal is in the midaspect of the acromion. This portal is established by palpating the soft interval between the posterior edge of the clavicle and anterior edge of the scapular spine. A line is drawn from this point laterally past the acromial edge by 2 to 3 cm. A spinal needle is used to verify the appropriateness of the portal before making a skin incision. Accessory Superolateral Portal This portal is used for placement of suture anchors and for tying knots and suture shuttling. It is placed just lateral to the anterior corner of the acromial edge. A spinal needle is used to localize the portal (Fig. 16-5). It is important that this portal allow for the appropriate dead man’s angle for suture anchor placement within the greater tuberosity.
Posterior Portal This is the first portal to be created in most arthroscopic cases. Although precise measurements have been described to locate the posterior portal, we recommend relying on palpation of the landmarks instead. Using the Romeo three-finger shuck, the index finger of the same hand as the shoulder being operated on is placed in the soft spot between the clavicle and scapular spine. The middle finger is placed on the coracoid, and the thumb feels the interval between the infraspinatus and teres minor. This helps the surgeon find the best and softest location of the posterior portal. If the posterior portal is to be used primarily as a viewing portal, using direct suture-passing methods from the lateral portal, the surgeon may choose to place this portal superiorly and laterally to allow improved visualization during cuff repair. Anterior Portal The anterior portal is generally placed in the triangular space in the rotator interval formed by the humeral head, subscapularis muscle, and intra-articular portion of the
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Figure 16-5. Proper positioning for anchor placement. A spinal needle is used to localize the current position for placement of the superolateral accessory portal to allow the proper position for anchor placement.
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SURGICAL TECHNIQUES Diagnostic Arthroscopy In all cases, diagnostic glenohumeral arthroscopy is initially performed, and any intra-articular pathology is addressed. The rotator cuff can then be visualized to confirm the presence of a full-thickness tear and to provide an initial estimation of the size and configuration of the tear.
Subacromial Inspection and Decompression Once the glenohumeral inspection is complete, the arthroscope is placed in the subacromial space. This is achieved by angling the trocar superiorly until it passes just under the posterior acromion. The trocar is then angled anteriorly and laterally to enter the subacromial bursa. The arthroscope is reintroduced to verify the location of the trocar. A “room with a view” is achieved when the arthroscope is inside the bursal sac. If the view is not seen, the arthroscope may be too anterior or medial, and this procedure should be repeated if necessary.
adequate visualization of the posterior tear margins. At this point, a standard arthroscopic acromioplasty is completed using the cutting block technique.
Preparation of Tuberosity Insertion Site To enhance healing of the torn tendon to the bone insertion site, the bone should be prepared with gentle débridement to achieve a bleeding bony surface (Fig. 16-6). This can be accomplished while viewing through the posterior portal, using a burr or bone-resecting shaver through the lateral portal. Bone preparation should begin just off the articular margin and proceed laterally to re-create the normal 10- to 15-mm footprint for rotator cuff insertion. Care must be taken to avoid decortication because this could compromise fixation strength of the suture anchors.
Determination of Tear Configuration and Repair
Working from the lateral portal, a thorough débridement of bursal tissue is performed using a standard 5.0-mm shaver to allow visualization of the tear. Care must be taken to débride all bursal tissue thoroughly anteriorly, posteriorly, and within the lateral gutter, because soft tissue remnants may swell during the remainder of the procedure and can impede visualization.
At this point, the arthroscope is placed into the lateral portal to allow direct visualization of the tear and determine tear configuration. Accurate identification of tear patterns is extremely important to achieve anatomic repair of the rotator cuff. Anatomic repair minimizes stress on the repair during the postoperative period and maximizes the chance of tendon healing. Finally, the technique used to repair each type of tear varies slightly, and accurate tear pattern recognition is imperative so that the most appropriate repair configuration can be selected.
Once débridement is completed from the lateral portal, we prefer to switch the arthroscope to the lateral portal. Next, working from the posterior portal using the shaver, care is taken to remove any remaining posterior bursa to allow
Crescenteric Tears For small single-tendon tears, the crescenteric pattern is most commonly encountered. This pattern represents detachment of the cuff from the tuberosity with minimal
A
B
Figure 16-6. Bone preparation. A, A high-speed burr or bone-cutting shaver is used to decorticate the tuberosity repair site lightly to create bleeding bone for tendon healing. Care must be taken to avoid significant bone resection, which could compromise anchor fixation. B, Completed bone bed can be checked for adequate bleeding by decreasing the pump pressure and visualizing an adequate bleeding bony surface.
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retraction (Fig. 16-7A). The tear is easily reduced to the greater tuberosity with little tension and can be directly repaired to bone. Repair of crescenteric tears begins with appropriate placement of the accessory anterolateral portal using spinal needle localization, as described earlier. Next, the first suture anchor is placed at the most posterior aspect of the tear. Suture anchor placement may be facilitated by humeral rotation and abduction. Anchors should be placed 5 to 10 mm lateral to the articular surface and should be separated by 5 to 8 mm. Anchors are sequentially placed in a posterior to anterior direction. Once the anchor has been placed, a penetrator is placed through the posterior portal (Fig. 16-8). The device is used to penetrate the cuff tissue a minimum of 5 mm medially to the tear edge. The penetrator is then used to grasp one limb of the posterior suture and pass it through the torn cuff and out of the posterior portal. This step is repeated
A
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for one limb of the second suture. The free ends of the sutures are then retrieved out through the posterior portal using a crochet hook. At this point, sutures can be stored on a hemostat and tied after all anchors are placed, or they can be tied immediately. The advantage of delaying suture tying until all sutures are passed is that the tendon remains mobile, which allows easier passage of subsequent sutures. However, multiple sutures in the space can cause confusion and difficulties with suture tangling. At this point, additional anchors are placed anteriorly as needed, and sutures are passed using a similar technique. However, the most anterior portion of the tear is usually not reachable using a penetrator from the posterior portal. In this case, a curved spectrum from the posterior portal or a straight spectrum from the anterior portal can be used (Fig. 16-9). When shuttling sutures using a spectrum-type device, three of the four sutures from the anchor are brought out through the anterior or posterior portal, whichever one is not being used for the spectrum. Only one suture now
B
C Figure 16-7. Arthroscopic views from the lateral portal. A, Crescenteric-type tear. B, U-shaped tear. C, L-shaped rotator cuff tear.
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a complete repair that is stable throughout the normal range of motion (Fig. 16-10).
Figure 16-8. Suture penetrator-type device. This device can be used from the posterior portal to penetrate the torn tendon and retrieve one limb of the suture from the anchor.
remains in the accessory anterolateral portal. A curved spectrum through the posterior portal or straight spectrum through the anterior portal is then used to pierce the anterior portion of the torn cuff. A monofilament suture is then passed and retrieved out through the anterolateral portal. The monofilament suture is tied around the anchor suture and then used to shuttle the anchor suture through the torn cuff. This process is repeated for the second anchor suture. At this point, all sutures are tied, working from a posterior to anterior direction. The tear is then inspected and the arm taken through internal and external rotation to ensure
Figure 16-9. A curved spectrum from the posterior portal can be used to shuttle sutures through the anterior aspect of the tear. (Courtesy of ConMed Linvatec, Largo, Fla.)
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An alternate technique for suture passage involves direct suture-passing devices, such as the EXPRESSEW (DePuy Mitek, Raynham, Mass) or Scorpion (Arthrex, Naples, Fla). When using these devices, the scope is placed in the posterior or an accessory posterolateral portal for viewing because the lateral portal is required for suture management. A 6- or 8.25-mm cannula is placed in the direct lateral portal and suture anchors are placed percutaneously through an accessory superolateral portal. Using this technique, anchors are placed from anterior to posterior. After anchors are placed, the most medial and anterior limb of the first suture is brought out through the lateral portal and loaded into the suture passer. The tissue is then grasped and the suture directly passed using the device (Fig. 16-11). The suture is then brought out through the anterior portal using a grasper and the process is repeated for the second suture. Finally, the free limbs of the suture are transferred from the anterolateral portal to the anterior portal, where all four strands of suture from a single anchor are placed on a hemostat. When using this technique, suture tying must be delayed until all sutures are passed because tying sutures early impedes the ability to pass the device under the torn edge of the rotator cuff to pass subsequent sutures. Multiple anchors can be placed by repeating the same technique. Finally, sutures are tied in a posterior to anterior direction through the lateral portal to minimize suture tangling. U-Shaped Tears U-shaped tears occur as tears become larger and retract further medially (see Fig. 16-7B). The hallmark of a U-shaped tear is the inability to reduce these tears to
Figure 16-10. Completed repair of a crescenteric-type tear when viewed from the lateral portal.
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Side-to-side sutures can be placed using direct antegrade passing or a hand-off technique. In direct antegrade passing, a penetrator device is loaded with a suitable nonabsorbable suture. While viewing from the lateral portal, the penetrator is placed through the posterior portal and penetrates the posterior leaf of the tear, followed by the anterior leaf of the tear. A suture retriever is then used through the accessory anterolateral portal to retrieve the suture from the anterior leaf. The penetrator is removed and the suture retriever is again used from the anterolateral portal to retrieve the suture from the posterior leaf. The suture can then be tied from the anterolateral portal, reducing the anterior and posterior leaves of the tear. Additional sutures can be placed laterally as needed.
Figure 16-11. Direct suture-passing device used to pass a loop of suture in an antegrade fashion from the direct lateral portal. A grasper seen in the background is then used to retrieve the loop through the anterior portal.
the tuberosity without undue tension on the repair. Anterior to posterior mobility in these tears is commonly maintained. These tears are initially managed with a margin convergence technique using side-to-side sutures (Fig. 16-12). Placement of these sutures causes the free margin of the torn cuff to converge laterally toward the tuberosity insertion site, allowing eventual repair of the tendon to bone while minimizing tension on the repair site (Fig. 16-13).
Using the hand-off technique, the scope is again placed in the direct lateral portal. A penetrator is loaded with suture and placed through the posterior portal and then through the posterior leaf of the tear. A second free penetrator is then placed through the anterior portal and pierces the anterior leaf of the tear. The suture is handed off from the posterior to the anterior penetrator and brought out through the anterior portal. A suture retriever is used to retrieve the posterior and anterior ends of the suture out through the anterolateral portal, where it can be tied. Once all side-to-side sutures have been placed, the tear can be repaired primarily using the technique described for crescenteric tears. It may be helpful to place the sutures from the anchors medially to the side-to-side
Method 3 Method 2
3A
2A
Method 4 4A
2B
3B 4B
Method 1 1A C 1B D E
Figure 16-12. Diagrammatic representation of techniques used to place margin convergence sutures during repair of U-shaped tears.
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A
B
Figure 16-13. Repairing U-shaped tears. A, View from lateral portal of side-to-side suture placed through the anterior and posterior leaves of the tear. B, After tying, the anterior and posterior leaves are reduced and the tear edge is moved laterally.
sutures. This results in a Mac stitch configuration, which has been shown to improve strength at the suture-tissue interface.7 L-Shaped Tears L-shaped tears occur when the rotator cuff tears off the tuberosity with extension of the tear along the anterior rotator interval (see Fig. 16-7C). Less commonly, the tear may have an extension posteriorly in the interval between the supraspinatus and infraspinatus. Tears with anterior extension result in retraction of the torn tendon in a posterior and medial direction. The important step in repairing these tears is to reduce the corner of the tear initially, bringing it anteriorly and laterally so that the anterior and posterior leaves of the tear are aligned. Once this has been completed, the intertendinous split can be repaired in a side-to-side fashion, converting the tear into a crescenteric pattern, which can be repaired to the tuberosity as described earlier. As these tears become chronic, they assume a more U-shaped configuration. In these cases, it is important to identify the tears as an L-shaped pattern by identifying which leaf, anterior or posterior, is more mobile and easily reduced. The first step in the repair of these tears is to reduce the more mobile leaf of the tear to the opposite side, thus reducing the tendon and creating a crescenteric tear. This can be done by placing a suture anchor and reducing the corner of the tear, or by placing side-to-side sutures along the longitudinal split. Our preference is to place the initial anchor at the corner of the L portion of the tear to reduce the tendon anatomically. Once this anchor has been placed, we use penetrators through the anterior and posterior portals to place one limb of each suture through one
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leaf of the tear, and then the second limb through the opposite leaf of the tear. This creates a horizontal mattress to secure the tendon to bone and reduce the anterior and posterior leaves together. These sutures may be tied immediately, although this may complicate subsequent suture passage. If this is done, sutures or a stay stitch may be used for provisional reduction while the remaining sutures are passed to ensure that anchor sutures are passed through the appropriate location in the tendon. Next, additional side-to-side sutures are placed along the longitudinal split as necessary to complete this portion of the repair. Once completed, the tear now assumes a crescenteric pattern. Additional sutures anchors are then used in the greater tuberosity to complete the repair in standard fashion.
POSTOPERATIVE REHABILITATION In general, rehabilitation after arthroscopic rotator cuff repair can be divided into three phases focusing on restoration of passive motion, restoration of active motion and, finally, strengthening of the shoulder (Appendix 16-1). However, the rehabilitation program for a rotator cuff tear should not be a standard protocol, but should be customized based on factors such as patient age, tear size, tissue quality, and security of repair. Any concomitant procedures performed may also need to be considered. In the initial phase, restoration of passive motion and prevention of stiffness constitute the primary goals. Although it has been documented that early active range of motion will help restore normal shoulder kinematics, it is
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important to take the risk of compromising the surgical repair into consideration. The patient is maintained immobilized in a sling with a small abduction pillow for the initial 6 weeks. Passive motion is initiated after the first postoperative visit; this includes Codman’s exercises, external rotation at the side, and forward elevation in the scapular plane. These exercises should be performed with the patient supine, the arm at the side, and the elbow bent. This reduces the forces across the shoulder and decreases the effect of gravity by shortening the lever arm of the upper extremity.
between open and arthroscopic repairs of the rotator cuff is the amount of discomfort experienced early by the arthroscopic patients. Less pain early enables patients to tolerate their range-of-motion exercises more readily. However, it is important not to accelerate the rehabilitation of arthroscopic patients because of their comfort levels. In all cases, the biology of repair has to be given time to work.
Pain is one of the key elements in deterring the restoration of motion. Therefore, it is important to provide pain relief during the rehabilitation phase of treatment. This can include rest, medications, avoidance of painful movements, cryotherapy, ultrasound, and galvanic stimulation.8 Once the pain and discomfort are controlled, motion exercises can be initiated.
When evaluating the results of arthroscopic rotator cuff repairs, important factors include pain relief and clinically based scoring scales, recovery of objective strength measures, and radiographic evaluation of tendon healing. Although many studies have reported excellent clinical results, there are only limited data on objective tendon healing, which we think is the most important factor in predicting strength recovery. Finally, most series involve primarily older patients. We are not aware of any specific studies on the outcome of rotator cuff repair in competitive athletes.
At 6 weeks postoperatively, immobilization is discontinued and active range of motion is allowed. During this phase, the emphasis is on restoring symmetrical passive range of motion and progressing to normal active range of motion. Significant strengthening is avoided until 12 weeks postoperatively. Light rotator cuff, deltoid, and scapular isometrics can be initiated at 8 weeks postoperatively. Furthermore, it is important to initiate the strengthening of scapular stabilizers and other endurance exercises for the entire body early. With progressive recovery, more aggressive measures can be taken for strengthening the injured shoulder. At 12 weeks after surgery, we initiate aggressive strengthening of the shoulder, beginning with isometrics and progressing to Thera-Bands (Hygenic Corporation, Akron, Ohio), and finally light weights. Strength training should be restricted to three times weekly to minimize pain and aggravation of the repair site. Internal and external rotation exercises should be performed in the scapular plane because they put minimal stress on the joint capsule. The most functional open-chain exercises are plyometrics activities. They help the muscle recover its strength and power. The muscle is initially stretched eccentrically and then slowly loaded. Examples of plyometrics exercises include the use of Thera-Bands, medicine balls, and free weights. Sports-related rehabilitation is initiated at 5 months postoperatively. Throwing is delayed until 6 months postoperatively, with throwing from a mound delayed until about 9 months. We allow a return to contact sports at 9 months. Patients should expect maximal improvement to occur at about 12 months postoperatively. It is important to stress that the biology of repair of rotator cuff muscles is the same regardless of the method used (open versus arthroscopic). The most noticeable difference
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RESULTS AND OUTCOMES
Several studies have reported favorable clinical results after arthroscopic rotator cuff repairs. Bennett9 has reported the results of arthroscopic repairs of 24 small to medium-sized tears. Overall, 100% of patients were satisfied with their outcome and all had significant improvements in terms of pain relief and function. Burkhart and associates10 have reported the results of 59 rotator cuff tears repaired arthroscopically. The patients had 95% good to excellent results, and results were independent of the size of the tear and whether margin convergence sutures were used. Moreover, the delay from injury to surgery did not adversely affect surgical outcome. A large retrospective study by Wolf and coworkers11 has reviewed the results of 96 rotator cuff arthroscopic repairs after 4 to 10 years. Of the patients available for re-evaluation, 94% had good to excellent results using the UCLA shoulder rating scale. Gartsman and colleagues12 have followed 73 patients for a minimum of 2 years who were treated arthroscopically for full-thickness rotator cuff tears. Of their patients, 84% rated their results as good or excellent. Significant improvement was seen in range of motion, strength, and in the results of the SF-36 shortform health survey. These studies involved the general population. Because rotator cuff tears are rarely seen in younger athletes, few studies have focused on this population and the ability of those patients to return to their sporting activities. SonneryCottet and colleagues13 followed 51 middle-aged tennis players with rotator cuff tears for 57 months, with the following results: 42 patients underwent open repair and 9 patients underwent arthroscopic débridement, and 80% of patients were able to return to playing tennis with no difference between the open and arthroscopic groups.
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More recently, some studies have reported the extent of tendon healing after arthroscopic rotator cuff repairs. Boileau and associates14 followed 65 patients with fullthickness rotator cuff tears treated arthroscopically for an average of 29 months. Computed tomography (CT) arthrography and magnetic resonance imaging (MRI) were used to assess the extent of tendon healing. Of these patients, 71% completely healed radiographically and the remainder did not, but showed a smaller defect size. Overall, 93% of patients were satisfied with their surgery, regardless of their tendon healing. However, those patients who had radiographic evidence of healing had better forward elevation strength. Another unpublished study by Verma and coworkers used ultrasound to check the integrity of arthroscopic and mini-open rotator cuff repairs (personal communication). The patients were followed for a minimum of 2 years. Using ultrasound, the failure rate of the mini-open group was 24% and that of the arthroscopic group was 25%. Smaller tears had a lower rate of failure, 17% in the mini-open and 19% in the arthroscopic group. Wilson and associates15 used second-look arthroscopy to evaluate the healing of 33 patients with rotator cuff repairs. The rotator cuff healed completely in 67% of patients. Future directions of arthroscopic rotator cuff repair are focused on improving the rates of tendon healing. Promising techniques include double-row fixation, which can increase the repair footprint and may improve the chances of healing.16 In most cases, however, failure of healing is likely the result of a biologic failure rather than failure of fixation. Therefore, the application of select biologic stimulators of soft tissue healing, such as growth factors, will likely play an important role in the future of rotator cuff repair surgery.
7. MacGillivray JD, Ma CB: An arthroscopic stitch for massive rotator cuff tears: The Mac stitch. Arthroscopy 20:669-671, 2004. 8. Kibler WB, Livingston B, Chandler TJ: Current concepts in shoulder rehabilitation. Adv Oper Orthop 3:249-301, 1996. 9. Bennett WF: Arthroscopic repair of full-thickness supraspinatus tears (small to medium): A prospective study with 2- to 4- year follow-up. Athroscopy 19:249-256, 2003. 10. Burkhart SS, Danaceau SM, Pearce CR Jr: Arthroscopic rotator cuff repair: Analysis of results by tear size and by repair technique—margin convergence versus direct tendon-to-bone repair. Arthroscopy 17:905-912, 2001. 11. Wolf EM, Pennington WT, Agrawal V: Arthroscopic rotator cuff repair: 4- to 10-year results. Arthroscopy 20:5-12, 2004. 12. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 13. Sonnery-Cottet B, Edwards TB, Noel E, Walch G: Rotator cuff tears in middle-aged tennis players: Results of surgical treatment. Am J Sports Med 30:558-564, 2002. 14. Boileau P, Brassart N, Watkinson DJ, et al: Arthroscopic repairs of full-thickness tears of the supraspinatus: Does the tendon really heal? J Bone Joint Surg Am Am 87:1229-1240 2005. 15. Wilson F, Hinov V, Adams G: Arthroscopic repair of fullthickness tears of the rotator cuff: 2- to 14- year follow-up. Arthroscopy 18:136-144, 2002. 16. Kim DH, Elattrache NS, Tibone JE, et al: Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med 34:407-414, 2006.
References 1. Lo IKY, Burkhart SS: Current concepts in arthroscopic rotator cuff repair. Am J Sports Med 31:308-324, 2003. 2. Millstein ES, Snyder SJ: Arthroscopic management of partial, full-thickness and complex rotator cuff tears: Indications, techniques and complications. Arthroscopy 19:189-199, 2003 3. Burkhart SS, Diaz Pagan JL, Wirth MA, Athanasiou KA: Cyclic loading of anchor-based rotator cuff repairs: Confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy 13:720-724, 1997. 4. Burkhart SS: Technical note: The dead man theory of suture anchor: Observation along a south Texas fence line. Arthroscopy 11:119-123, 1995. 5. Burkhart SS, Fischer SP, Nottage WM, et al: Tissue fixation security in transosseous rotator cuff repairs: A mechanical comparison of simple versus mattress sutures. Arthroscopy 12:704-708, 1996. 6. Lo IKY, Burkhart SS, Chan KC, Athanasiou KA: Arthroscopic knots: Determining the optimal balance of loop security and knot security. Arthroscopy 20:489-502, 2004.
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APPENDIX 16-1 Rehabilitation After Arthroscopic
Rotator Cuff Repair
4. Motion—shoulder a. Passive only i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction b. Codman’s pendulum exercises to promote early motion 5. Motion—elbow a. Passive and active flexion and extension b. Passive and active supination and pronation 6. Muscle strengthening a. Grip strengthening only 7. Progress to phase II if: a. 6 weeks of recovery b. Painless passive range of motion to: i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction
Phase I (weeks 0-6) 1. Restrictions a. No active or active-assisted range of motion i. Small tears (0-1 cm): No active forward flexion for 6 weeks ii. Medium tears (1-3 cm): No active range of motion for 6 weeks iii. Large tears (3-5 cm): No active range of motion for 8 weeks iv. Massive tears (⬎5 cm): No active range of motion for 12 weeks b. Passive range-of-motion exercises allowed i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction c. No strengthening until 12 weeks after surgery i. In young healthy patients with small acute tears, isometric exercises can be initiated at 8 weeks. 2. Immobilization a. Amount of abduction depends on tear and what is required to keep tension on repair at a minimum i. Sling only (if there is minimal tension on repair) 1. Small tears: 1-3 weeks 2. Medium tears: 3-6 weeks 3. Large or massive tears: 6-8 weeks ii. Abduction pillow (tension minimized with arm at 20-40 degrees of abduction) 1. Small tears: 6 weeks 2. Medium tears: 6 weeks 3. Large tears: 8 weeks 3. Pain control a. Medications i. Narcotics for 7-10 days after surgery ii. Nonsteroidal anti-inflammatory drugs (NSAIDs) for patients with discomfort beyond first 10 days b. Therapeutic modalities i. Moist heat before therapy, ice after therapy ii. Ultrasound iii. Galvanic stimulation
Phase II (weeks 6-12) 1. Restrictions a. No strengthening or resisted range of motion until 12 weeks after surgery b. No active range of motion for massive tears 2. Immobilization a. Discontinue sling or abduction pillow b. Use for comfort only 3. Pain control a. NSAIDs b. Therapeutic modalities 4. Motion—shoulder a. Goals i. 140-160 degrees of forward flexion ii. 40-60 degrees of external rotation iii. 60-90 degrees of abduction b. Exercises i. Continue with passive range of motion ii. Begin active-assisted range of motion iii. Progress to active range of motion iv. Light passive stretching at the end ranges of motion 5. Muscle strengthening a. Only for small nondisplaced tears i. Can advance to light Thera-Band for internal and external rotation ii. Can begin scapular stabilizers 189
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6. Progress to phase III if: a. Painless active range of motion b. No shoulder pain Phase III (months 3-6) 1. Goals a. Improve shoulder strength, power, and endurance b. Improve shoulder proprioception c. Establish a home maintenance program performed three times/week d. Stretching exercises daily 2. Motion a. Achieve motion equal to contralateral side b. Passive capsular stretching at end ranges of motion, including cross-body adduction and internal rotation to stretch posterior capsule 3. Strengthening a. Begin with closed-chain isometric exercises i. Internal rotation ii. External rotation iii. Abduction iv. Forward flexion v. Extension b. Progress to open-chain exercises with Thera-Bands i. Exercises with elbow bent to 90 degrees ii. Start with shoulder at 0 degrees of forward flexion, abduction, and external rotation iii. Arc of 45 degrees in each of five planes of motion
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iv. Progress through six color-coded bands v. Progression to next level band occurs at 2- to 3-week intervals vi. Thera-Bands permit isotonic eccentric and concentric shoulder strengthening vii. Progress to isotonic dumbbell exercises in all five planes c. Strengthening of deltoid (especially anterior) d. Strengthening of scapular stabilizers i. Closed-chain 1. Scapular retraction (rhomboids, middle trapezius) 2. Scapular protraction (serratus anterior) 3. Scapular depression (latissimus dorsi, trapezius, serratus) 4. Shoulder shrugs (trapezius, levator scapulae) ii. Progress to open-chain 4. Functional strengthening a. Begin after 70% of strength recovered b. Plyometrics 5. Return to sport a. Sport-specific exercises (e.g., throwing, golfing, tennis) 6. Maximum improvement a. Small tears (4-6 months) b. Medium tears (6-8 months) c. Large tears (8-12 months) d. Patients will continue to show improvements in function for at least 1 year.
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CHAPTER 17 Anterior Instability
of the Shoulder Samuel A. Taylor, Mark C. Drakos, and Stephen J. O’Brien
wrestling and 332,000 in soccer.3 Anterior shoulder dislocation is a common affliction of young active patients, often precipitated by a sports-related injury. Given the number of high school students alone participating in such sports and the traumatic nature of anterior glenohumeral dislocation, it is not surprising that the average age of patients seen for evaluation of anterior shoulder instability is younger than 28 years.4-9
Joint laxity does not indicate shoulder instability; rather, there are varying degrees of laxity in the normal shoulder.1,2 When a patient presents with glenohumeral instability, it is important to differentiate normal laxity from instability clinically and to establish the primary direction of instability. Patients should be separated clinically into two groups, those suffering from symptomatic laxity and those demonstrating overt instability of the glenohumeral joint. Furthermore, determining the positions and activity in which clinical instability occurs also provides useful information during the evaluation.
Young active patients presenting with an acute anterior dislocation of the glenohumeral joint who are treated nonoperatively re-dislocate at rates as high as 80% to 90%.7,10,11 It is our belief that young athletes who desire to return to their sport and present with acute anterior shoulder dislocation should be treated surgically.
Athletes experiencing symptomatic laxity may present with problems stemming from repetitive edge loading, traction on the glenoid labrum or biceps labral complex, rotator cuff tendinitis, or dead arm symptoms resulting from traction on the brachial plexus as the lax shoulder subluxes inferiorly or anteroinferiorly. A typical example of symptomatic laxity is the football lineman who develops posterior pain and labral injuries that result from blocking with the arms forward-flexed and elbows locked in extension. Additionally, baseball pitchers are particularly susceptible to exacerbations of internal impingement from symptomatic laxity. This is caused by tremendous forces incurred by the soft tissue structures surrounding the glenohumeral joint during the production of the throwing arc with the humerus abducted and externally rotated. Repetitive motions such as these stress the surrounding soft tissue structures, including the glenohumeral ligaments and supraspinatus rotator cuff tendon. The resulting microtrauma and tension can lead to refractory tendinitis and potentially to labral injuries caused by the supraspinatus tendon becoming impinged between the humerus and glenoid. Effectively, a pathologic cycle develops in which repetitive stress magnifies the glenohumeral laxity; this in turn contributes to internal impingement.
As our surgical technique and collective acumen continue to advance treatment options and prognoses for patients with anterior glenohumeral instability, a fundamental understanding of the anatomy and pathoanatomy of the glenohumeral joint is absolutely critical to the diagnosis and surgical treatment of overt anterior shoulder instability in the athlete. This point is emphasized by the field’s departure from nonanatomic techniques of stabilization, such as the Bristow, Putti-Platt, and Magnuson-Stack procedures. We believe that the most effective stabilization techniques focus on restoration of normal glenohumeral anatomy, particularly through repair and proper tensioning of the inferior glenohumeral ligament complex. Such intervention allows not only for stability, but some tailoring can be done to allow for the recovery of desired function in the throwing and nonthrowing athlete.
ANATOMY OF THE STABLE AND UNSTABLE SHOULDER The human shoulder joint (Fig. 17-1) is formed by the humeral head and glenoid surface of the scapula. As humans developed an orthograde posture, the glenohumeral joint evolved so that the head of the humerus abuts the glenoid fossa, as opposed to articulating within. Whereas this anatomic relation affords the glenohumeral joint tremendous flexibility and range of motion, it does so at the cost of biomechanical stability.12 Unlike other joints, the articulating surface area of the shoulder is limited. The biomechanical stability of the shoulder is reliant on two types of anatomic restraints, dynamic
In contrast to symptomatic laxity, overt instability refers to problems in which the athlete is unable to contain the humeral head within the glenoid fossa and it clearly dislocates, leaving the athlete in a fully compromised position, vulnerable to more serious nerve, bone, or joint injuries, until the shoulder is reduced. The focus of this chapter will be on those individuals who demonstrate overt anterior or anteroinferior instability. In 2001, it was reported that over 1 million U.S. high school students participated in football, almost 250,000 in 191
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Figure 17-1. Sagittal view of the glenohumeral joint.
and static, which work cooperatively to maintain glenohumeral stability by generating joint compressive forces and directing the net force through the humeral head into the glenoid fossa.13 Static stabilizers are unable to generate force and include the bony structures of the humeral head and glenoid fossa, the fibrous glenoid labrum, and several capsuloligamentous structures.14-16 Static mechanisms of stabilization provide the greatest contribution to glenohumeral stability at the extreme ranges of motion, because they remain lax through the midrange of motions13 and become taut as the shoulder approaches its normal limits of motion.17 Dynamic stabilizers include the muscles of the rotator cuff, the deltoid group, pectoralis major, and latissimus dorsi, and are therefore a critical component to glenohumeral stability. Concavity compression is a force that acts to contain the humeral head in the glenoid fossa and is a function of the depth of the articulating fossa (provided by the glenoid and the labrum) and forces generated by the surrounding musculature that direct the humeral head into the glenoid. In addition to generating compressive forces, dynamic stabilizers also initiate movement that leads to tightening of capsuloligamentous structures.14,18-20 The glenoid fossa is shaped like an inverted comma, with average measurements of 35 mm vertically and 25 mm transversely.21,22 Saha’s studies21-23 also noted an average of 7.4 degrees of glenoid retroversion in 75% of shoulders and 2 to 10 degrees of anteroversion in the remaining 25% of shoulders. The hemispherical surface of the humeral head—radii of curvature, 25 mm vertically and 22 mm transversely12—is designed to interact with the shallow concave surface of the glenoid (2.5 mm anteroposteriorly and 9 mm superoinferiorly)24 so that the contact surface area is maximized. Articular interaction is enhanced by the inclination of the humeral head with respect to the shaft and the retrotorsion.25 Saha22 has separated glenohumeral
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joints into three groups based on the radius of curvature of the glenoid fossa and radius of the humeral head. Type A articulation is defined by a humeral head radius smaller than that of the glenoid, Type B joints exhibit similar radii for the two surfaces, and type C articulation has a larger humeral head radius than glenoid radius. Interactions between a humeral head and glenoid fossa with differences in radii approaching zero (type B) are inherently the most stable because the contact surface area is maximized. However, Soslowsky and colleagues26 have claimed that in 88% of cases, the glenoid and humeral head exhibit less than a 2-mm difference in radii, suggesting that most glenohumeral joints could be considered type B; thus, inequality in radii of curvature fails to explain most anterior instability cases. The anatomic neck of the humerus also plays a crucial role in glenohumeral stability because it serves as an attachment site for the glenohumeral capsule and the glenohumeral ligaments (see later). The concept of osseous adaptation has been explored and documented in professional baseball pitchers27 and professional European handball players28; it was found that the dominant arm develops significant glenoid retroversion in the dominant arm. During the act of throwing, with the humerus in 90 degrees abduction and external rotation, tremendous forces are applied to the static and dynamic stabilizers of the shoulder. Osseous adaptation is the concept that the glenoid fossa adopts a modified bony conformation to accommodate the repetitive stress of the throwing motion. Thus, anterior stability of the shoulder is enhanced through the increased articular surface area present throughout the throwing arc. The glenoid labrum is dense fibrous tissue with a triangular shape that encircles the glenoid rim and attaches directly to the long head of the biceps tendon at the supraglenoid tubercle (Fig. 17-2). The labrum contributes greatly to glenohumeral stability by deepening the glenoid fossa,29 without changing the curvature of the glenoid.30 Lippitt and associates31 have demonstrated the labrum’s contribution to stability by showing that its resection leads to a 20% decrease in resistance to translation. Furthermore, the labrum increases the surface area in contact with the humeral head, and serves as an attachment point for the glenohumeral capsule and ligaments. The contribution of the shoulder capsule to stability depends on collagen integrity, attachment sites on the glenoid and humeral head, and position of the arm. The glenohumeral capsule consists of three layers,15 is less than 5 mm thick,32 and shows significant individual variation. The anterior capsule is more substantial than the thin posterior capsule; it is composed of loose areolar connective tissue33 and predominantly type I collagen.34 The primary role of the capsule in glenohumeral stabilization is to maintain negative intra-articular pressure. A capsular or
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ANTERIOR INSTABILITY OF THE SHOULDER
193
L
G hh Figure 17-2. Glenoid labrum (L). This is a triangularly shaped rim of dense fibrous tissue that acts mechanically to deepen the glenoid fossa and increase the surface area of the articulating glenoid (G) and humeral head (hh).
labral defect, such as is the case in a Bankart lesion (see later) results in a loss of the negative intra-articular pressure35 critical to the maintenance of shoulder stability through the midranges of motion. The glenohumeral ligaments are discrete thickenings of the glenohumeral capsule, identifiable grossly and histologically (Fig. 17-3). The most common cause of anterior shoulder instability is insufficiency of these capsuloligamentous structures. A thorough understanding of the anatomy, histology, and biomechanics of these structures is crucial to understanding and treating anterior shoulder instability. Turkel and coworkers36 have laid the groundwork for the study of these static contributions, by showing that in 0 degrees of abduction, anterior stability is maintained by the subscapularis tendon, in 45 degrees abduction the shoulder is stabilized by the subscapularis tendon, middle glenohumeral ligament, and anterior fibers of the inferior glenohumeral ligament, and in 90 degrees abduction and external rotation the inferior glenohumeral ligament provides stabilization. The superior glenohumeral ligament has been identified in 90% to 97% of specimens investigated.15,37,38 It takes its origin at the supraglenoid tubercle, just anterior to the insertion of the long head of the biceps tendon, and inserts into the anatomic neck to the humerus slightly superior to the lesser tuberosity. The superior glenohumeral ligament is also a component of the rotator interval39 (see later). The ligament’s size and integrity vary from person to person and are not easily visualized arthroscopically. The superior glenohumeral ligament contributes little to anteroposterior stability of the shoulder;40 however, it acts in concert
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Figure 17-3. Glenohumeral ligaments. This sagittal view represents an anatomic illustration of the glenohumeral ligaments and inferior glenohumeral ligament complex. A, anterior; AB, anterior band; AP, axillary pouch; B, long head biceps tendon; IGHLC, inferior glenohumeral ligament complex; MGHL, middle glenohumeral ligament; P, posterior; PB, posterior band; PC, posterior capsule; SGHL, superior glenohumeral ligament. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 26.)
with the coracohumeral ligament to limit inferior glenohumeral translation41 with the arm adducted or in the neutral position. The coracohumeral ligament is an extracapsular structure that courses from the lateral surface of the coracoid process to the greater and lesser tuberosities straddling the bicipital groove. The coracohumeral ligament aids the superior glenohumeral ligament in limiting inferior glenohumeral translation. Together, these two ligaments contribute greatest to stability when the arm is adducted or in 0 degrees abduction.16 As the arm is abducted to 90 degrees, the mechanical contribution of these ligaments to stability decreases progressively to zero, at which point the ligaments are slack. The middle glenohumeral ligament demonstrates even greater variability in its attachment, size, and integrity than the superior glenohumeral ligament. When the ligament is present, it typically originates just inferior to the superior glenohumeral ligament at the supraglenoid tubercle or at the same level from the glenoid neck and inserts into the humerus just medial to the lesser tuberosity.25 The thickness of the middle glenohumeral ligament has been found to vary tremendously, from a thick well-defined structure to a gossamer thickening of the anterior capsule.42 Additionally,
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this glenohumeral ligament has been shown to be absent in 27% of shoulders.15 Although the middle glenohumeral ligament’s contribution to glenohumeral stability varies in accordance with its size and integrity, studies have found that its primary function is to restrain inferior translation when the arm is adducted and externally rotated.16 It also works as an accessory stabilizer to anterior translation following damage to the anterior band of the inferior glenohumeral ligament complex when the arm is abducted to 90 degrees.40 The inferior glenohumeral ligament complex is perhaps the most critical for the prevention of dislocation in an abducted shoulder40,43 and surgical intervention for anterior glenohumeral instability (Fig. 17-4). Selective sectioning experiments15,29,36,44 have helped elucidate the inferior glenohumeral ligament’s role as the most important static stabilizer of the glenohumeral joint anteriorly. As O’Brien and colleagues15 have delineated, the inferior glenohumeral ligament complex consists of three distinct components—the anterior band, axillary pouch, and posterior band. Together, these three components make up what has been referred to as a hammock-like structure that offers anterior, posterior, and inferior stability to the abducted glenohumeral joint. Anatomically, the anterior band takes its origin from between the 2- and 4-o’clock positions on the face of the glenoid (Fig. 17-5).15 Histologic examination has revealed that the anterior band of the inferior glenohumeral ligament’s attachment to the glenoid is facilitated by direct attachment of collagen fibers to the labrum and by collagen fibers that interact directly with the bone.45 Meanwhile, the posterior band of the inferior glenohumeral ligament complex takes its origin from between the 7- and 9-o’clock
Posterior
Anterior
Figure 17-4. View of the attachment sites for the anterior and posterior bands of the inferior glenohumeral ligament complex of the glenoid. Note that the anterior band attaches higher up on the comma-like glenoid than the posterior band and that their attachment sites define the hammock-like structure of the complex.
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positions along the face of the glenoid and has been shown to be less consistent than either the anterior band or the axillary pouch in its structure and function.46 Histologically, the inferior glenohumeral ligament complex consists of three layers, similar to the structure of the shoulder capsule described earlier. However, the perpendicularly oriented fiber pattern within the three layers of the inferior glenohumeral ligaments makes it easy to differentiate it from the capsule. Both the anterior and posterior bands consist of easily distinguishable, abrupt, and well-organized collagen bundles visualized as thickenings of the innermost layer. In between the anterior and posterior bands lies the thickest section, the axillary pouch, which similarly runs from the glenoid to the humerus and is continuous with the other two elements of the inferior glenohumeral ligament complex anteroposteriorly. Histologically, however, the axillary pouch differs from the anterior and posterior bands in the orientation of its collagen fibers. O’Brien and associates15 noted in their landmark paper that the collagen fibers of the axillary pouch are not synchronously aligned, but rather are less well organized and exhibit mixing of fibers from the inner and middle layers of the capsule, making differentiation difficult. More recently, however, others have described the collagen fiber pattern of the axillary pouch to be more organized than originally proposed, to have a radial pattern in the ligament’s midsubstance,47 and to have a multiaxial fiber orientation that is somewhat similar to that seen in the anterior and posterior bands.48 Bigliani and coworkers19 have determined that the tensile strength of each of the three components of the inferior glenohumeral ligament is comparable when corrected for thickness and surface area, supporting the notion that the axillary pouch consists of equally organized collagen fibers. The anterior band, axillary pouch, and posterior band have been shown to be thicker toward their glenoid origin than laterally at their humeral insertions.46 Furthermore, the three components of the inferior glenohumeral ligament complex exhibit similar length, about 43 mm, despite the differences in their thickness, structure, and sites of origin and insertion. The inferior glenohumeral ligament complex, which originates between 2 and 9 o’clock on the face of the glenoid, follows two separate insertion patterns on the humerus: (1) a collar-like attachment in which the entire complex inserts along the same circumferential ring, slightly inferior to the articular margin of the humeral head; and (2) a V-shaped attachment, which gleans its name from the shape that results when the anterior and posterior bands attach just inferior to the articular margin, and the axillary pouch attaches further inferiorly (Fig. 17-6).15 As mentioned earlier, the three components of the inferior glenohumeral ligament complex act in concert as the primary stabilizer of the abducted shoulder through their hammock-like action around the axis of rotation (Fig. 17-7).
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195
B
A
C Depending on the position of the arm, the inferior glenohumeral ligament complex can stabilize against anterior, posterior, and inferior translation. As the arm is abducted to 90 degrees, the inferior glenohumeral ligament complex tightens beneath the humeral head and acts as the main stabilizer against inferior translation, because the nature of
A B C
Figure 17-6. Attachment sites of the glenohumeral ligaments. Left, the superior glenohumeral ligament inserts into the fovea capitis line just superior to the lesser tuberosity (A). The middle glenohumeral ligament inserts into the humerus just medial to the lesser tuberosity (B). The inferior glenohumeral ligament complex has two common attachment mechanisms (C). It may attach in a collar-like fashion, or it may have a V-shaped attachment to the articular edge (right). (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 18.)
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Figure 17-5. Anterior band of the inferior glenohumeral ligament. A, Example of a collar-like attachment of the inferior glenohumeral ligament complex just inferior to the articular edge and closer to the articular edge than the remainder of the capsule. B, V-shaped attachment of the inferior glenohumeral ligament complex of the humerus, with the axillary pouch attaching to the humerus at the apex of the V farther from the articular edge. C, Inferior glenohumeral ligament complex (IGHLC). This is thicker than the anterior capsule (AC) and posterior capsule (PC). (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 21.)
the superior glenohumeral ligament renders it slack and ineffective at this degree of abduction. O’Brien and colleagues40 have demonstrated anteroposterior translation of the glenohumeral joint to be greatest when the abducted arm is at 0 degrees of extension. Furthermore, they have shown that the anterior band of the glenohumeral ligament complex is the primary mechanism for resisting anteriorposterior translation with the abducted arm in the neutral position or in 30 degrees of extension as the anterior band becomes taut. However, when the 90-degree abducted arm is moved into 30 degrees of forward flexion, the anterior band becomes slack, allowing the now taut posterior band to bear the burden of stabilizing the glenohumeral joint against anterior-posterior translation. Similarly, the hammock-like action of the inferior glenohumeral ligament complex (Fig. 17-8) acts to stabilize this diarthrodial joint further when the abducted humerus is externally rotated. In such a position, the anterior band and axillary pouch fan out anteriorly to provide support to the humeral head and stabilize the joint against anterior translation.49 Conversely, the same is true of the posterior band and axillary pouch, which provide posterior support to the internally rotated abducted arm as fibers of the posterior band and axillary pouch fan out posteriorly to cradle the humeral head and resist posterior instability. Although of a variable thickness,15,19,50 the inferior glenohumeral ligament complex is continuous with the remainder of the shoulder capsule anteriorly and posteriorly.
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II 90˚ Abd.
M
amm
k oc
C
A
c
H
M
am
ck
A
H
C
H
H
a
K
K
d
mo
O
M
O
M
B
A
A
E.R. I.R.
C
D
Figure 17-7. Hammock-like action of the inferior glenohumeral ligament complex. A, The inferior glenohumeral ligament complex is tightened during abduction (Abd.). B, During abduction and internal (c) or external rotation (d), different parts of the band are tightened (a, c, d). C, With internal rotation (I.R.), the posterior band fans out to support the head and the anterior band becomes cordlike or relaxed, depending on the degree of horizontal flexion or extension. D, With abduction and external rotation (E.R.), the anterior band fans out to support the head and the posterior band becomes cordlike or relaxed, depending on the degree of horizontal flexion or extension. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 20.)
Continuity of this hammock-like structure with the rest of the shoulder capsule is tremendously important because it allows us to consider the inferior glenohumeral ligament complex as a hammock within a hammock (see Fig. 17-8). That is, action can be taken surgically at various places in the shoulder capsule that will affect (tightening or loosening) the hammock-like action of the inferior glenohumeral ligament complex. This surgical approach, particularly through manipulation of the rotator interval, allows the surgeon to exploit the hammock within a hammock concept in a way that restores anterior stability to the ailing patient. (See later,“Surgical Techniques To Correct Anterior Instability,” for further discussion of this topic.) The final anatomic component that demands attention is the rotator interval. The rotator interval (Fig. 17-9) is a term first used by Neer51 to describe a triangular area defined medially by the coracoid process, superiorly by the anterior border of the supraspinatus tendon, and inferiorly by the superior aspect of the subscapularis tendon.52 The contents of this triangular space include the coracohumeral
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C
B
Figure 17-8. Schematic illustration of the thickened portion of the inferior glenohumeral ligament complex (IGHLC) as it exists in continuum with the remainder of the shoulder capsule. The anatomic relation leads to the concept of a hammock within a hammock, which maintains that actions taken on the glenohumeral capsule outside the IGHLC, such as surgical closure of the rotator interval, and will have a secondary effect of tightening of the IGHLC as it relates to stability. A, The glenoid fossa with its surrounding muscular and ligamentous attachments are seen in the sagittal view, demonstrating that the IGHLC (hammock) sits within the greater glenohumeral capsule (HAMMOCK). B, Sutures can be placed to close the rotator interval, which in turn tightens the capsule (HAMMOCK) and IGHLC (hammock). C, Closure of the rotator interval has the effect of raising and tightening the IGHLC (hammock).
SS
g
CP
hh
ST
Figure 17-9. Rotator interval. The rotator interval is seen here in an extra-articular anterior-posterior view through subdeltoid arthroscopy. The triangular space is anatomically defined superiorly by the supraspinatus tendon (SS), medially by the coracoid process (CP), and inferiorly by the subscapularis tendon (ST). The humeral head (hh) is seen as it articulates within the glenoid fossa (g).
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an r io
rb
d an rb rio te An d
Axillary pouch
an
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te Po s
Posterior translation
rb
Before discussing these pathologic lesions and their surgical treatment in detail, it is first important to understand the extent of the damage caused by an anterior dislocation of the shoulder. It is best to think of the capsuloligamentous structures spanning the glenoid and humeral head as being continuous, similar to a circle, just like the previously described hammock within a hammock concept. In such a model, damage to anterior and posterior structures is present, even though anterior instability predominates clinically (Fig. 17-10). Anterior dislocation, therefore, results in two traumas: (1) anterior damage typically manifested as a Bankart lesion; and (2) reciprocal posterior capsuloligamentous laxity from damage to the hammock. Therefore, it is common for cases of anterior
Axillary pouch
r io
A number of pathologic lesions have been identified that result in or contribute to anterior shoulder instability. Subfailure strain on the inferior glenohumeral ligament complex and the resulting microtrauma, anteroinferior labral lesions (Bankart lesions), rupture injury to the inferior glenohumeral ligament complex, and bone defects are all common pathologic consequences of the violent forces imposed on the joint during athletic activities.
ri
te
An
te
PATHOLOGIC LESIONS AND ANTERIOR INSTABILITY
d
an
b or
s Po
ligament, superior glenohumeral ligament, middle glenohumeral ligament, and long head of the biceps tendon, which runs through the intertubercular groove.53 Jost and associates39 have further elucidated the layers of the rotator interval through a series of dissections. They determined that the rotator interval space is actually two parts differentiated by the number of tissue layers. One part is defined as lateral to the cartilage bone transition and consists of four layers—superficial fibers of the coracohumeral ligament, fibers of the supraspinatus tendon and subscapularis tendon, deep fibers of the coracohumeral ligament, and fibers of the superior glenohumeral ligament and joint capsule. The other more medial part of the rotator interval covers the cartilaginous humeral head and consists of only two layers, the coracohumeral ligament and the superior glenohumeral ligament and joint capsule. Operative experience has revealed that the thickness and composition of the rotator interval are highly variable and can be visualized arthroscopically, ranging from a thick strong barrier to an almost translucent wispy structure invariably unable to offer structural support beyond maintenance of negative intra-articular pressure. Such anatomic variability was demonstrated by Cole and coworkers53 in 2001 when they evaluated the rotator interval regions from 37 fetuses and 10 fresh-frozen cadavers, demonstrating that the inner capsular layer of 75% of the rotator intervals studied lacks a continuous link of loosely associated collagenous connective tissue; instead, it is covered only by a thin synovial membrane.
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d
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Axillary pouch Anterior translation
Figure 17-10. Circle concept. This can be regarded as a means to understanding the role of the shoulder capsule in shoulder stability. Damage to both sides of the capsule is required to produce dislocation in one direction.
shoulder instability to manifest clinically with some degree of posterior laxity. Similarly, anterior laxity will accompany posterior dislocation. This concept has been reinforced by studies that have revealed anterior and posterior injury of the capsule resulting from a unidirectional trauma in the cadaveric shoulder.54-56 Speer and colleagues57 have demonstrated with a cadaveric model that anteroinferior labral injury increases the amount of anterior glenohumeral translation by a mean of 3.4 mm. They deemed this degree of translation minimal, unable to account for anterior dislocation of the joint on its own, and suggested that other anatomic abnormalities, especially capsular stretching, must be present to permit the humeral head to dislocate anteriorly. A Bankart lesion typically occurs as a result of anterior humeral head dislocation. It is defined as a detachment of the anteroinferior glenoid labrum, with its attached anterior band of the inferior glenohumeral ligament complex. A Bankart lesion causes a decrease in the tension of the anterior band and thus reduces the ligament’s ability to retain the humeral head in the glenoid fossa, especially with the arm in positions of glenohumeral vulnerability. It is important to reiterate that as the shoulder reaches 90 degrees of abduction with external rotation, the primary restraints to anterior translation are the anterior band and axillary pouch of the inferior glenohumeral ligament complex, which fan anteriorly.40 In 90 degrees of abduction and forward flexion, the anterior band becomes slack, whereas the posterior band tightens and acts to prevent anterior translation. Therefore, to restore stability to the glenohumeral joint, even in the case of anteroinferior avulsion of the glenoid labrum, competency and proper tensioning of all three components of the inferior glenohumeral ligament complex must be re-established. Two other types of injury to the inferior glenohumeral ligament complex can occur in the athlete’s shoulder, rupture
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of the ligament and subfailure injury resulting in elongation stretching of capsuloligamentous tissues. There are three potential sites of failure for the inferior glenohumeral complex: (1) at the glenoid insertion; (2) in the ligament’s midsubstance; and (3) at the humeral insertion point. During unidirectional testing, studies have indicated that 40% of specimens rupture at their glenoid origin (Bankart lesion), 35% fail in the midsubstance, and 25% fail at the humeral insertion.19 Wolf and colleagues58 have looked arthroscopically at 64 shoulders with diagnosed anterior instability and found that just 9.3% of patients present with a humeral avulsion of the inferior glenohumeral ligament complex anteriorly, 17.2% of patients demonstrate generalized capsular laxity, and the overwhelming majority of patients, 73.5%, present with a primary Bankart lesion. Malicky and associates58 have demonstrated through a new technique that stress on the anteroinferior capsule yields variable force vectors with a multiaxial representation. Furthermore, their biomechanical analysis showed that the highest levels of strain on the anteroinferior capsule are near the ligament’s glenoid insertion as opposed to near the humeral insertion. Although the most common pathology seen in anterior instability is certainly a primary Bankart lesion, it is important to rule out humeral insertion failures58 through arthroscopic visualization or radiographic imaging. Variable subfailure stresses encountered by the glenohumeral joint have been implicated in stretching of the associated capsuloligamentous structures. Bigliani and coworkers19 have in fact noted significant elongation of the inferior glenohumeral ligament complex. Pollock and colleagues61 have determined, through exposure of the inferior glenohumeral ligament to several different levels of subfailure stress, that repetitive loads similar to those experienced by athletes result in ligament elongation and joint laxity. Moreover, they speculated that this unrecoverable ligamentous elongation might be the end product of accumulated microdamage to the ligament tissues. This concept was used by Remia and associates62 to stretch the capsuloligamentous structures of the shoulder to 20% beyond their original length to create a model of generalized glenohumeral laxity with increased rotation and translation for analysis of various surgical techniques. Bone pathology associated with anterior instability is not uncommon. The Hill-Sachs lesion occurs on the posterior aspect of the humeral head as a result of the violent collision between the posterior humeral head and anterior glenoid rim during anterior dislocation. A Hill-Sachs lesion that interacts with the anterior glenoid rim when the arm is in 90 degrees abduction and external rotation has been termed an engaging Hill-Sachs lesion by Burkhart and De Beer63 and noted to be a contraindication for arthroscopic stabilization. They also described a glenoid in which the bone has been ground down anteroinferiorly as an inverted pear glenoid and noted this as another contraindication to arthroscopic
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repair. Sugaya and associates64 have used three-dimensional reconstructed computed tomography (CT) to evaluate 100 shoulders of patients with recurrent anterior glenohumeral instability. They found that osseous Bankart lesions are present in 50% of cases. Additionally, 40% of patients had scans consistent with erosion or compression of the anterior glenoid rim.
SURGICAL TECHNIQUES TO CORRECT ANTERIOR INSTABILITY Historically, the methods for the surgical correction of anterior glenohumeral shoulder instability have fallen into one of two distinct genres—anatomic reconstruction or nonanatomic reconstruction. Anatomic reconstruction focuses on restoring normal anatomy to the shoulder joint by addressing pathology associated with dislocation. To be effective, anatomic reconstruction must pay particular attention to the hammock-like inferior glenohumeral ligament complex. Conversely, the emphasis of nonanatomic approaches is to construct new structures to contain the humeral head and thus prevent anterior dislocation. Effective primary surgical treatment of anterior shoulder instability lies in anatomic reconstruction, particularly when addressing any pathoanatomy associated with the inferior glenohumeral ligament complex.
Open Repair Techniques A Bankart lesion is the most common surgical finding in patients with anterior instability. As such, the open Bankart repair is traditionally considered to be the gold standard for the surgical treatment of anterior shoulder instability. In the classic study by Rowe and colleagues,65 a long-term review of 145 patients treated with open Bankart repairs was conducted; results indicated only a 3.5% recurrence rate, with 69% of patients able to achieve full range of motion. The hallmark of the Bankart repair is restoration of tension to the anteroinferior capsule and inferior glenohumeral ligament complex. To address these structures, the surgeon must enter the capsule vertically and medially to the inferior rim of the glenoid. Removal of soft tissue attachments to the glenoid precedes the drilling of three holes in the glenoid, through which sutures are passed to facilitate the superomedial advancement of the inferior capsule and anterior band of the inferior glenohumeral ligament complex. Such superomedial advancement of these structures restores tension to the hammock-like complex. This technique, however, is often ineffective for treating anteriorly dislocating patients with excessive capsular laxity or for treating multidirectional instability patients who primarily dislocate anteriorly. Treating these patients requires a form of capsular shift (Fig. 17-11). Neer and Foster66 have described an inferior capsular shift in which
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stabilization, anchor fixation, and thermal capsulorrhaphy. Failure rates of these procedures vary among studies, and the relative indications for arthroscopic stabilization versus open stabilization will be discussed elsewhere in this text (Chapter 21).
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Figure 17-11. Neer capsular shift. A, Lateral and vertical incisions are made in the lax capsule. B, The lax capsule is then imbricated, improving tension and removing capsular redundancy.
lax capsular tissue is addressed via lateral and vertical incisions through the capsule (see Fig. 17-11A) at the humeral neck and advanced laterally and superiorly (see Fig. 17-11B), thus removing capsular redundancy. Recommended Open Technique T-plasty modification of the Bankart repair has been described by Altchek and associates67 as a method to correct multidirectional instability (Fig. 17-12). In this technique, both a transverse incision in the capsular midsubstance and a vertical incision along the glenoid margin are used (see Fig. 17-12A). The latter incision is used first to inspect the joint for a Bankart lesion and then to repair that lesion, if present (see Fig. 17-12B). The transverse incision affords the ability to advance the inferior flap superiorly and the superior flap inferiorly to imbricate the capsule, thereby reducing joint laxity.
Arthroscopic Repair Tremendous advancements have been made in the arthroscopic treatment of anterior shoulder instability since Johnson and Bayley68 introduced the arthroscopic application of metal staples as a method for repairing a Bankart lesion. Today, many arthroscopic methods have been described in the literature, including transglenoid arthroscopic
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B
Before beginning any arthroscopic procedure, a complete examination under anesthesia should be performed comparing the injured shoulder with the contralateral shoulder, because such an assessment is often difficult to perform on the awake patient. Once the arthroscope is introduced into the injured shoulder, a thorough arthroscopic evaluation of the status of the inferior glenohumeral ligament complex, labrum, rotator cuff, and any bony lesions that may be present should be performed. In addition to these two procedures, the arthroscopic drivethrough sign69-71 is often a valuable intraoperative tool for assessment of glenohumeral laxity. The arthroscopic drivethrough sign is the ability to maneuver the arthroscope in between the humeral head and the glenoid fossa at the level of the anterior band of the inferior glenohumeral ligament complex. McFarland and coworkers72 have evaluated the clinical significance of the drive-through sign and its pertinence to the diagnoses of various shoulder abnormalities. They examined 234 shoulders arthroscopically and found that the drive-through sign has a high sensitivity (92%) and negative predictive value (94.2%), but low specificity (37.6%) for glenohumeral instability. Their results indicate that a positive drive-through sign should be used in conjunction with other diagnostic criteria in determining shoulder instability, because it is not in itself specific to the pathology. Although the diagnosis of anterior shoulder instability may not accurately be made using this sign, it is our clinical experience that elimination of a positive arthroscopic drive-through sign intraoperatively is a good predictor of proper tensioning of the hammock-like inferior glenohumeral ligament complex (Fig. 17-13). Arthroscopic staple capsulorrhaphy, in which a metal staple is used to repair a Bankart lesion, described in 1982 by
Figure 17-12. T-plasty modification of Bankart repair. A, The transverse and vertical incisions allow access to the joint for a Bankart repair. B, The capsule can then be imbricated to reduce joint laxity.
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g
hh
g hh
A
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Figure 17-13. Positive arthroscopic drive-through sign. A, Viewed from the standard posterior portal. The drive-through sign can be seen when the surgeon can maneuver the arthroscope between the glenoid (g) and the humeral head (hh). B, Removal of the arthroscopic drive-through sign after surgical intervention may help estimate proper correction of anterior shoulder instability.
Johnson and Bayley, was the first in a series of arthroscopic techniques developed to address pathology associated with anterior dislocation of the glenohumeral joint. Reported rates of recurrent dislocation and subluxation in the literature are high. Johnson and Bayley, in fact, have reported a recurrence rate of 21%.68 Lang and colleagues73 have evaluated 54 shoulders at an average of 39 months, describing a 33% occurrence of postoperative instability, loose staples in 15% of patients, and less than 50% of treated athletes able to return to overhead sporting activities. Furthermore, Coughlin and associates74 have described a 25% failure rate among the 47 patients they followed at 4 years postoperatively. Because of the substantial failure rates and the occurrence of some articular injuries associated with loose hardware, staple capsulorrhaphy has been essentially abandoned in favor of newer techniques that attempt to ameliorate these pitfalls.
is freed to the 6-o’clock position, followed by reattachment of the Bankart lesion,78 with proper reattachment and tensioning of the inferior glenohumeral ligament complex. Arciero and coworkers79 have reported on 19 military cadets followed at a mean of 19 months, all of whom were treated with bioabsorbable anchor fixation, and there was only one recurrence of subluxation (5%). In this study, all athletes were able to return to preinjury levels of performance and 94.7% indicated a Rowe score of good or excellent. Other studies in the literature have reported failure rates of 10%,7 15%,80 and 3.2%.81 Although their results are promising, Cole and colleagues82 have emphasized the importance of patient selection for bioabsorbable anchor fixation, with the prime candidate being an individual with a relatively healthy capsule and only a Bankart lesion resulting from traumatic anterior dislocation.
The evaluation of arthroscopic stabilization has included numerous other techniques, such as thermal capsulorrhaphy and anchor fixation. Thermal capsulorrhaphy uses the application of thermal energy75,76 to “shrink” the capsule by altering the capsular collagen architecture. Although this technique was widely embraced by orthopedic surgeons in the late 1990s because it appeared to offer a quick and effective intervention for management of the unstable shoulder, it has since fallen out of favor specifically because of the variability of the host reaction and its failure to address the primary pathologic process, the Bankart lesion. We believe that thermal capsulorrhaphy is not indicated for the treatment of anterior shoulder instability and that the issues of capsular redundancy are more effectively addressed through closure of the rotator interval.
Recommended Arthroscopic Technique Suture anchors are the preferred method for arthroscopic repair of anterior glenohumeral instability, because this technique offers the safest and most accurate method for repairing a Bankart lesion. As with any arthroscopic procedure for shoulder instability, examination under anesthesia should be performed to compare the injured shoulder with the contralateral shoulder to determine the direction and extent of humeral translation. Furthermore, diagnostic arthroscopy is a useful tool for evaluation of the inferior glenohumeral ligament, labrum, rotator cuff, and any bony lesions that may be present.
Anchor fixation stabilization is an arthroscopic technique that uses a cannulated spike to repair Bankart lesions. Both bioabsorbable and fixed anchors have been used to this end, each with their own pull-out specifics that must be taken into account.77 The surgical technique requires an initial stripping of the glenoid neck so that the labrum
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With the patient in the beach chair position (Fig. 17-14), the glenoid neck is first stripped so that the labrum is mobilized to the 6-o’clock position. Once this has been accomplished, anchors are screwed into the glenoid rim and sutures are passed at the 5-, 4-, and 3-o’clock positions. The capsuloligamentous tissue is then secured to the anchors via sutures that are tied sequentially, so that proper tension is restored to the inferior glenohumeral ligament complex.83
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Figure 17-14. Beach chair position. This position allows for easy access to the structures that need to be addressed during arthroscopic correction of anterior shoulder instability, including access to the subdeltoid space.
Although suture anchors offer an accurate means of addressing the pathologies of anterior instability, they are not without risk. Eight cases of suture anchor migration were reported by Kaar and associates84 in 2001, reaffirming the importance of anchor placement and indicating the potential risks associated with implantation of this type of hardware. Rotator interval closure is frequently an integral component of the surgical correction of anterior shoulder instability (Fig. 17-15). As noted, the rotator interval is a triangular space bordered medially by the coracoid process, inferiorly by the subscapularis tendon, and superiorly by the supraspinatus tendon. Field and coworkers85 have selectively closed the rotator interval in patients with isolated rotator interval lesions and associated inferior instability and noted
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good or excellent results in all patients. Manipulation of the rotator interval, in addition to an arthroscopic Bankart repair, can be a powerful tool, allowing the surgeon to remove capsular redundancy, especially in patients with an inferior component to their instability. The inferior glenohumeral ligament complex functions as a hammock-like structure that supports the humeral head throughout a wide range of glenohumeral motion. The inferior glenohumeral ligament complex sits within and is continuous with the remainder of the joint capsule—hence, the hammock within a hammock concept. Thus, closure of the rotator interval indirectly tightens the inferior glenohumeral ligament complex. Suture anchor Bankart repair, in conjunction with rotator interval closure, allows the surgeon to address the instability and, more importantly, preserve a patient’s functional needs.
Nonanatomic Reconstructions Several nonanatomic surgical repairs of anterior glenohumeral instability have been described over the years. The general goal of nonanatomic methods of repair is to stabilize the glenohumeral joint by creating physical obstacles to humeral translation. Nonanatomic repairs come in three different forms: (1) subscapularis muscle alteration procedures; (2) suspensory procedures; and (3) bone block procedures. Although some of these nonanatomic techniques have been reported to have positive results in terms of prevention of further shoulder dislocations and patient satisfaction,86,87 many associated complications have been associated with these types of repairs, such as recurrent anterior dislocations, restricted motion, and premature osteoarthritis.86-92 Moreover, nonanatomic procedures leave the shoulder’s anatomy altered, leading to increased difficulty for the surgeon in addressing the joint if future revision surgeries become
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D
Figure 17-15. Rotator interval closure. The exposed rotator interval (A) is viewed in an anterior to posterior direction through the subdeltoid space. Sutures are passed arthroscopically (B, C) to oppose the edges of the supraspinatus and subscapularis tendons, resulting in surgical closure (D) of the rotator interval. A subdeltoid approach to such a closure allows for extra-articular knot placement, as seen here.
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necessary.93,94 It is our experience, therefore, that the surgical complications mentioned, along with the failure to address the inferior glenohumeral ligament complex, render nonanatomic approaches ineffective and an inappropriate first line of defense against glenohumeral instability. However, for historical purposes, we will briefly outline some of these nonanatomic procedures. Two procedures have been used by orthopedists that involve alteration of the subscapularis muscle. The PuttiPlatt procedure (Fig. 17-16) involves both—shortening the subscapularis muscle through its division and subsequent reattachment and reinforcement of the anterior joint through a reattachment that creates overlap of the muscle’s divided ends.95 Similarly, the Magnuson-Stack procedure attempts to produce stability by advancing the subscapularis tendon laterally, reattaching it to a point on the humerus just lateral to the bicipital groove.96
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Two suspensory procedures, the Nicola97,98 and Gallie99 procedures, are noteworthy. The former uses the long head of the biceps tendon as a suspensory ligament and the latter uses a graft of fascia lata to suspend the humeral head. Finally, two bone block procedures have been described. The Bristow-Latarjet procedure uses a transfer of the distal end of the coracoid process, including the insertion of the conjoint tendon, to the inferior portion of the glenoid rim, thus preventing anterior humeral translation.100,101 The Eden-Hybbinette102,103 procedure functions via much the same concept—namely, blocking anterior translation of the humerus using a bone block. Both procedures can result in early osteoarthritis and restrictions in range of motion, have been linked to complications arising from the implanted hardware,104,105 and can further complicate revision surgery because of significant scarring.93
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Ongoing Debate: Open Versus Arthroscopic Stabilization Despite the data that exist regarding recurrence rates, postoperative morbidities, and a narrowing of the gap between open and arthroscopic stabilization failure rates,106 the decision to pursue one of these two types of stabilization procedures must ultimately be based on what is best for a particular patient. In their 2000 studies, Cole and colleagues107,108 concluded that the outcome differences between open and arthroscopic repair are negligible in the surgical management of traumatic instability of the shoulder if patients are selected appropriately, based on observed intraoperative pathoanatomy. Ultimately, a physician who begins an arthroscopic stabilization should never fear conversion to an open repair because “a good open procedure will always outperform a bad arthroscopic one.”94 Green and Christensen’s 1993 study109 evaluated common surgical morbidities in 38 patients who had Bankart repairs
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C Figure 17-16. Putti-Platt procedure. Subscapularis tendon is divided (A), reattached in overlapping fashion (B), and imbricated (C) at the anterior joint to reinforce the joint and improve anterior glenohumeral stability. (From Osmond-Clark H: Habitual dislocation of the shoulder: The Putti-Platt operation. J Bone Joint Surg 30B:19-25, 1948.)
(20 arthroscopic, 18 open). They found significant decreases in operative time, blood loss, postoperative narcotic use, hospital stay, postoperative fevers, and time lost from work as compared with patients who underwent an open Bankart repair. Today, most arthroscopic stabilization patients are ambulatory. Moreover, as arthroscopic techniques and collective surgical acumen continue to evolve, these morbidities are certain to show continued improvements.
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The open Bankart repair is the gold standard for anterior instability treatment and has typically had low failure rates.65 Pagnani and Dome110 have followed 58 American football players at an average time point of 37 months post–open Bankart repair and found that only 3.4% of patients experienced a recurrent subluxation, 94.8% were rated as excellent or good, and 89.6% were able to return to playing their sport for at least 1 year. However, other studies have generated contradictory data. Uhorchak and associates111 have reported on 66 patients followed up at an average of 47 months; 23% experienced recurrent dislocation (3%), fewer than three postoperative subluxations (12%), or multiple recurrent subluxations (8%). Magnusson and coworkers112 have reported similarly high failure rates for open repair. Mohtadi and colleagues,113 however, came to the conclusion, through their metaanalysis, that “open repair has a more favorable outcome with respect to recurrence and return to activity.” The question must be asked as to whether an open Bankart repair is still the gold standard for treatment of anterior shoulder instability. Arthroscopic stabilization techniques have matured over the past 2 decades, as evidenced by reports of low failure rates and patient satisfaction. In a comprehensive study of the early evolution of arthroscopic shoulder stabilization, DeBarardino and associates7 have conducted an extensive study of 127 West Point cadets who experienced acute glenohumeral dislocations; 72 patients were treated with arthroscopic stabilization and evaluated by the authors in three cohorts determined by the time period in which the surgery was performed. They found that the first group of 9 cadets, treated with staple capsulorrhaphy between 1986 and 1988, showed a failure rate of 22.2%. The second group of 21 cadets, treated using transglenoid sutures between 1988 and 1991, demonstrated a failure rate of 14%. The final group of 42 cadets yielded a failure rate of only 10% and were treated with bioabsorbable tack fixation. This study is of particular note because it demonstrates the evolution from staple capsulorrhaphy to bioabsorbable anchor fixation and its associated decrease in failure rates, and because the cohorts were made up of young men (average age, 19.5 years) leading active lives. Not all reports have shown failure rates as low as 10%. In fact, other studies have reported highly variable failure rates, ranging from 0% to almost 50%.4-6,8,69,114-116 More recently, however, reports have indicated recurrence rates in arthroscopically treated patients that rival those seen in patients treated with the more traditional open Bankart repairs.106,117,118 Kim and coworkers117 have reported a recurrence rate of only 4% in 167 patients followed up at a mean of 44 months who had a suture anchor fixation. They cited Rowe scores of excellent or good in 95% of patients, with 91% of patients able to return to a preinjury levels of activity, and an average loss of only 2 degrees of external rotation.
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Contact athletes who present with anterior shoulder instability represent a very controversial subset of patients. Deciding whether these high demand patients should be managed with open surgical repair instead of arthroscopic repair remains a crux and is debated substantially in the literature. Hubbell and colleagues119 have reported on differences in arthroscopic and open repairs in collision athletes and found that 6 of 9 such athletes treated arthroscopically experienced “repeat instability,” whereas no such patients treated with an open repair developed a recurrence. Although patients treated with an open repair showed a lower rate of recurrence, the patients demonstrated restrictions in their range of motion, particularly that of external rotation. Based on their findings, it was recommended that collision athletes suffering from anterior shoulder instability should undergo an open repair, whereas athletes whose sport demands a more extensive range of motion, such as swimmers and throwers, should undergo arthroscopic repair. In contrast to the results of this study, other reports have suggested that arthroscopic repair of the unstable glenohumeral joint in collision and contact athletes is an acceptable means of intervention.120,121 Burkhart and DeBeer63 have described their results for 101 contact athletes who underwent arthroscopic Bankart repairs. Initial review of the results seems to be incomplete, because recurrence rates appear high. However, when the patients are segregated into two cohorts based on anatomic findings—(1) those who demonstrate an engaging Hill-Sachs lesion or an inverted pear glenoid, and (2) those not in the first group—the results are striking. The stratified results showed an 87% recurrence rate in group 1 and only a 6.5% recurrence rate for those in group 2. Burkhart and DeBeer’s study63 has demonstrated the importance of intraoperative decision making that best suits the patient. Although it is not our practice to exclude arthroscopic stabilization before entering the operating room, some have suggested contraindications to this procedure, which include an inverted pear glenoid or an engaging Hill-Sachs lesion,63 capsular defects, previously failed open or arthroscopic stabilizations, or previously failed thermal capsulorrhaphy.94,122 Ultimately, we believe that we can address anterior instability arthroscopically with equal or greater efficacy than through the use of an open technique for most patients. However, when unable to accomplish a satisfactory stabilization arthroscopically because of any of the aforementioned contraindications, we do not hesitate to convert to an open procedure. If a patient has an isolated Bankart lesion with unidirectional instability, arthroscopic failure rates today almost match those of open repairs. Failure rates, however, do not match in patients with multidirectional instability. Also, as discussed earlier, closure of the rotator interval is an important and useful method for reducing or eliminating capsular redundancy, especially when the patient has an inferior component to their instability.85
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Millet and colleagues94 have also prescribed humeral avulsion of the inferior glenohumeral ligament complex as a potential contraindication to arthroscopic stabilization because of difficulty in accessing the space adequately with current arthroscopic techniques. Pagnani and Dome110 have cited advantages to the open technique, including (1) being able to leave the arm in a position that facilitates surgery without having to worry about losing proper visibility, and (2) better extracapsular visualization of the rotator interval, with easier access for closure of this space, if necessary. Open technique offers access to and visualization of what current arthroscopic techniques cannot encompass, but what future techniques may allow.
Subdeltoid Arthroscopic Stabilization Subdeltoid arthroscopy was developed by Stephen J. O’Brien as a means of arthroscopically transferring the long head of the biceps tendon from its intra-articular origin at the supraglenoid tubercle to the extracapsular conjoint tendon on the coracoid process (Fig. 17-17).123 Subdeltoid arthroscopy allows for visualization of many anatomic structures that were once unviewable arthroscopically in a clear, welldistended field that can be easily maintained through saline insufflation for over 2 hours if necessary (Fig. 17-18). Verma and asssociates123 have briefly described reaching the subdeltoid space using careful dissection with a mechanical shaver and a radiofrequency device from the posterior
Figure 17-18. Subdeltoid space. This can be visualized through clearing of the fascial plane with a radiofrequency device while insufflating with normal saline.
portal after first moving anteriorly through the subacromial space. Within the fascial plane, the subdeltoid space is readily cleared with the same devices (Fig. 17-19). The resulting space, now distended with saline, allows direct visualization of many anatomic structures of the anterior shoulder and chest, previously seen only during open procedures, including the coracoid process, conjoint tendon, pectoralis major and minor, anterior capsule subscapularis tendon,
d
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Figure 17-17. Subdeltoid arthroscopy. The normal anatomy exposed by subdeltoid arthroscopy includes the anterior glenohumeral capsule, pectoralis major tendon, long head of the biceps tendon, conjoint tendon, coracoid process, coracohumeral ligament, supraspinatus tendon, and subscapularis tendon.
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Figure 17-19. Arthroscopic exposure of the subdeltoid space. This reveals a “room with a view” and allows the surgeon to view the coracoid process (cp), conjoint tendon (ct), deltoid muscle (d), pectoralis major muscle and tendon (pm), anteroinferior glenohumeral capsule (gc), and humerus (h) clearly. The anatomy is clearly defined from a posterior portal looking anteriorly in this right shoulder.
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supraspinatus tendon, and the rotator interval. In addition to reducing the bleeding, scarring, pain, and soft tissue damage associated with open procedures, we believe that when the subdeltoid space is distended with saline, visibility is actually greater than what can be achieved with an open technique because the surgeon can see more normal anatomic relationships. Furthermore, subdeltoid arthroscopy allows the surgeon to perform essentially the same gold standard operation as an open procedure. To date, Dr. O’Brien has performed several virgin and revision arthroscopic stabilizations using the subdeltoid space. These are exciting advances; subdeltoid arthroscopy will provide shoulder surgeons with another tool to address anterior shoulder pathology through less invasive means and obviate the need for open shoulder procedures.
REHABILITATION FOLLOWING ANTERIOR STABILIZATION Postoperatively, patients should be given limitations in range of motion for at least 3 weeks according to the goals set at the time of surgery. Because a baseball pitcher needs greater flexibility of the shoulder than a football linebacker, these two athletes’ recoveries should be tailored according to performance needs. The rehabilitative process begins with passive range-of-motion exercises, with progression to active assisted and finally to active range-of-motion and strengthening exercises. Successful rehabilitation often demands the involvement of a physical therapist who is knowledgeable and experienced in handling patients who have had recent anterior stabilization procedures. References 1. McFarland EG, Campbell G, McDowell J: Posterior shoulder laxity in asymptomatic athletes. Am J Sports Med 24: 468-471, 1996. 2. Harryman DT 2nd, Sidles JA, Harris SL, et al: Laxity of the normal glenohumeral joint: A quantitative in vivo assessment. J Shoulder Elbow Surg 1:66-76, 1992. 3. National Federation of State High School Associations: 2001 Athletic Participation Summary. Indianapolis, National Federation of State High School Associations, 2002. 4. Arciero RA, Taylor DC, Snyder RJ, Uhorchak JM: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 5. Grana WA, Buckley PD, Yates CK: Arthroscopic Bankart suture repair. Am J Sports Med 21:348-353, 1993. 6. Youssef JA, Carr CF, Walther CE, Murphy JM: Arthroscopic Bankart suture repair for recurrent traumatic unidirectional anterior shoulder dislocations. Arthroscopy 11:561-563, 1995. 7. DeBerardino TM, Arciero RA, Taylor DC: Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc 5:263-271, 1996.
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8. Speer KP, Warren RF, Pagnani M, Warner JJ: An arthroscopic technique for anterior stabilization of the shoulder with a bioabsorbable tack. J Bone Joint Surg Am 78:1801-1807, 1996. 9. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two- to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 10. Henry JH, Genung JA: Natural history of glenohumeral dislocation—revisited. Am J Sports Med 10:135-137, 1982. 11. Arciero RA, Wheeler JH, Ryan JB, McBride JT: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med 22:589-594, 1994. 12. O’Brien S, Fealy S, Drakos M, Botts J: Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In Rockwood CA Jr., Matsen FA III, Wirth MA, Lippitt SB (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 2004, pp 1-31. 13. Lippitt S, Matsen F: Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res (291):20-28, 1993. 14. Ferrari DA: Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20-24, 1990. 15. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 16. Warner JJ, Deng XH, Warren RF, Torzilli PA: Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med 20:675-685, 1992. 17. Bigliani LU, Kelkar R, Flatow EL, et al: Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res (330):13-30, 1996. 18. Bach BR, Warren RF, Fronek J: Disruption of the lateral capsule of the shoulder. A cause of recurrent dislocation. J Bone Joint Surg Br 70:274-276, 1988. 19. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 20. Blasier RB, Guldberg RE, Rothman ED: Anterior shoulder stability: Contribution of rotator cuff forcesand the capsular ligaments in a cadaver model. J Shoulder Elbow Surg 1: 140-50, 1992. 21. Saha AK: The classic. Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Clin Orthop Relat Res (173):3-10, 1983. 22. Saha AK: Theory of Shoulder Mechanism: Descriptive and Applied. Springfield, Ill, Charles C Thomas, 1961. 23. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491-505, 1971. 24. Howell SM, Galinat BJ: The containment mechanism: The primary stabilizer of the glenohumeral joint. Presented at the Annual Meeting of The American Academy of Orthopedic Surgeons. San Francisco, January 23, 1987. 25. Dugas JR, Cooper DE, O’Brien SJ: Gross and microscopic anatomy of the shoulder. In Warren RF, Craig EV, Altchek DW (eds): The Unstable Shoulder. Philadelphia, Lippincott-Raven, 1999, pp 27-50. 26. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop Relat Res (285):181-190, 1992. 27. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30:20-26, 2002.
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28. Pieper HG: Humeral torsion in the throwing arm of handball players. Am J Sports Med 26:247-253, 1998. 29. Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232, 1988. 30. Cooper DE, Arnoczky SP, O’Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am 74:46-52, 1992. 31. Lippitt SB, Vanderhooft JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quantitative analysis. J Shoulder Elbow Surg 2:27-35, 1993. 32. Ciccone WJ 2nd, Hunt TJ, Lieber R, et al: Multiquadrant digital analysis of shoulder capsular thickness. Arthroscopy 16:457-641, 2000. 33. Yamazaki S: Fibrous structure of the joint capsule in the human shoulder. Okajimas Folia Anat Jpn 67:127-139, 1990. 34. Rodeo SA, Suzuki K, Yamauchi M, et al: Analysis of collagen and elastic fibers in shoulder capsule in patients with shoulder instability. Am J Sports Med 26:634-643,1998. 35. Habermeyer P, Schuller U, Wiedemann E: The intra-articular pressure of the shoulder: An experimental study on the role of the glenoid labrum in stabilizing the joint. Arthroscopy 8:166-172, 1992. 36. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 37. Steinbeck J, Liljenqvist U, Jerosch J: The anatomy of the glenohumeral ligamentous complex and its contribution to anterior shoulder stability. J Shoulder Elbow Surg 7: 122-126, 1998. 38. DePalma AF, Callery G, Bennett GA: Variational anatomy and degenerative lesions of the shoulder joint. AAOS Instr Course Lect 6:255-281, 1949. 39. Jost B, Koch PP, Gerber C: Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg 9:336-341, 2000. 40. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298-308, 1995. 41. Levine WN, Flatow EL: The pathophysiology of shoulder instability. Am J Sports Med 28:910-917, 2000. 42. DeLorme D: Die Hemmungs bander des Schultergelenks and ihre Deductung fur die Schulter Luxationen. Arch Klin Chir (92):79, 1910. 43. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 44. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992 . 45. McMahon PJ, Dettling J, Sandusky MD, et al: The anterior band of the inferior glenohumeral ligament. Assessment of its permanent deformation and the anatomy of its glenoid attachment. J Bone Joint Surg Br 81:406-413, 1999. 46. Ticker JB, Bigliani LU, Soslowsky LJ, et al: Inferior glenohumeral ligament: Geometric and strain-rate dependent properties. J Shoulder Elbow Surg 5:269-279, 1996. 47. Gohlke F, Essigkrug B, Schmitz F: The pattern of the collagen fiber bundles of the capsule of the glenohumeral joint. J Shoulder Elbow Surg 3:111-128, 1994.
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48. Debski RE, Moore SM, Mercer JL, et al: The collagen fibers of the anteroinferior capsulolabrum have multiaxial orientation to resist shoulder dislocation. J Shoulder Elbow Surg 12:247-252, 2003. 49. Soslowsky LJ, Malicky DM, Blasier RB: Active and passive factors in inferior glenohumeral stabilization: A biomechanical model. J Shoulder Elbow Surg 6:371-379, 1997. 50. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 51. Neer CS 2nd: Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 52:1077-1089, 1970. 52. Bennett WF: Visualization of the anatomy of the rotator interval and bicipital sheath. Arthroscopy 17:107-111, 2001. 53. Cole BJ, Rodeo SA, O’Brien SJ, et al: The anatomy and histology of the rotator interval capsule of the shoulder. Clin Orthop Relat Res (390):129-137, 2001. 54. Curl LA, Warren RF: Glenohumeral joint stability. Selective cutting studies on the static capsular restraints. Clin Orthop Relat Res (330):54-65, 1996 . 55. Pagnani MJ, Warren RF: Stabilizers of the glenohumeral joint. J Shoulder Elbow Surg 3:173-190, 1994. 56. Warren RF, Kornblatt IB, Marchand R: Static factors affecting posterior shoulder stability. Orthop Trans 8:89, 1984. 57. Speer KP, Deng X, Borrero S, et al: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76:1819-1826, 1994. 58. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy 11:600-607, 1995. 59. Malicky DM, Kuhn JE, Frisancho JC, et al: Neer Award 2001. Nonrecoverable strain fields of the anteroinferior glenohumeral capsule under subluxation. J Shoulder Elbow Surg 11:529-540, 2002. 60. Malicky DM, Soslowsky LJ, Kuhn JE, et al: Total strain fields of the antero-inferior shoulder capsule under subluxation: A stereoradiogrammetric study. J Biomech Eng 123:425-431, 2001. 61. Pollock RG, Wang VM, Bucchieri JS, et al: Effects of repetitive subfailure strains on the mechanical behavior of the inferior glenohumeral ligament. J Shoulder Elbow Surg 9: 427-435, 2000. 62. Remia LF, Ravalin RV, Lemly KS, et al: Biomechanical evaluation of multidirectional glenohumeral instability and repair. Clin Orthop Relat Res (416):225-236, 2003. 63. Burkhart SS, De Beer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677694, 2000. 64. Sugaya H, Moriishi J, Dohi M, et al: Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am 85:878-884, 2003. 65. Rowe CR, Patel D, Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 66. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980.
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67. Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone Joint Surg Am 73:105-112, 1991. 68. Johnson JR, Bayley JI: Early complications of acute anterior dislocation of the shoulder in the middle-aged and elderly patient. Injury 13:431-434, 1982. 69. Pagnani MJ, Warren RF, Altchek DW, et al: Arthroscopic shoulder stabilization using transglenoid sutures. A four-year minimum follow-up. Am J Sports Med 24:459-467, 1996. 70. Peterson CA, Altchek DW, Warren RF: Operative arthroscopy. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 290-335. 71. Pagnani MJ, Warren RF: Arthroscopic shoulder stabilization. Oper Tech Sports Med 1:276-284, 1993. 72. McFarland EG, Neira CA, Gutierrez MI, et al: Clinical significance of the arthroscopic drive-through sign in shoulder surgery. Arthroscopy 17:38-43, 2001. 73. Lane JG, Sachs RA, Riehl B: Arthroscopic staple capsulorrhaphy: A long-term follow-up. Arthroscopy 9:190-194, 1993. 74. Coughlin L, Rubinovich M, Johansson J, et al: Arthroscopic staple capsulorrhaphy for anterior shoulder instability. Am J Sports Med 20:253-256, 1992. 75. Arnoczky SP, Aksan A: Thermal modification of connective tissues: Basic science considerations and clinical implications. Instr Course Lect 50:3-11, 2001. 76. Arnoczky SP, Aksan A: Thermal modification of connective tissues: Basic science considerations and clinical implications. J Am Acad Orthop Surg 8:305-313, 2000. 77. Fealy S, Drakos MC, Allen AA, Warren RF: Arthroscopic bankart repair: Experience with an absorbable, transfixing implant. Clin Orthop Relat Res (390):31-41, 2001. 78. Flik KR, Lopez V, Allen AA: Single-point fixation for shoulder instability. In Miller MD, Cole BJ (eds): Textbook of Arthroscopy. Philadelphia, Elsevier; 2004, pp 94-104. 79. Arciero RA, Taylor DC, Snyder RJ, Uhorchak JM: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 80. Karlsson J, Magnusson L, Ejerhed L, et al: Comparison of open and arthroscopic stabilization for recurrent shoulder dislocation in patients with a Bankart lesion. Am J Sports Med 29:538-542, 2001. 81. Segmuller HE, Hayes MG, Saies AD: Arthroscopic repair of glenolabral injuries with an absorbable fixation device. J Shoulder Elbow Surg 6:383-392, 1997. 82. Cole BJ, Romeo AA, Warner JJ: Arthroscopic Bankart repair with the Suretac device for traumatic anterior shoulder instability in athletes. Orthop Clin North Am 32:411-421, 2001. 83. Moskal MJ, Pearl ML: Suture anchor fixation for shoulder instability. In Miller MD, Cole BJ (eds): Textbook of Arthroscopy. Philadelphia, Elsevier, 2004, pp 105-112. 84. Kaar TK, Schenck RC Jr, Wirth MA, Rockwood CA Jr: Complications of metallic suture anchors in shoulder surgery: A report of 8 cases. Arthroscopy 7:31-37, 2001. 85. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557-563, 1995. 86. Hill JA, Lombardo SJ, Kerlan RK, et al: The modification of the Bristow-Helfet procedure for recurrent anterior shoulder subluxations and dislocations. Am J Sports Med 9:283-287, 1981.
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87. Hovelius L, Sandstrom B, Sundgren K, Saebo M: One hundred eighteen Bristow-Latarjet repairs for recurrent anterior dislocation of the shoulder prospectively followed for fifteen years: Study I—clinical results. J Shoulder Elbow Surg 13:509-516, 2004. 88. Rowe CR, Zarins B, Ciullo JV: Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am 66:159-168, 1984. 89. Hovelius L, Thorling J, Fredin H: Recurrent anterior dislocation of the shoulder. Results after the Bankart and PuttiPlatt operations. J Bone Joint Surg Am 61:566-569, 1979. 90. Fredriksson AS, Tegner Y: Results of the Putti-Platt operation for recurrent anterior dislocation of the shoulder. Int Orthop 15:185-188, 1991. 91. van der Zwaag HM, Brand R, Obermann WR, Rozing PM: Glenohumeral osteoarthrosis after Putti-Platt repair. J Shoulder Elbow Surg 8:252-258, 1999. 92. Rachbauer F, Ogon M, Wimmer C, et al: Gleohumeral osteoarthrosis after the Eden-Hybbinette procedure. Clin Orthop Relat Res (373):135-140, 2000. 93. Young DC, Rockwood CA Jr: Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am 73:969-981, 1991. 94. Millett PJ, Clavert P, Warner JJ: Open operative treatment for anterior shoulder instability: When and why? J Bone Joint Surg Am 87:419-432, 2005. 95. Osmond-Clarke H: Habitual dislocation of the shoulder: The Putti-Platt operation. J Bone Joint Surg Br 30:19-25, 1948. 96. Magnuson PB, Stack JK: Recurrent dislocation of the shoulder. JAMA 123:889-892, 1943. 97. Nicola T: Recurrent dislocation of the shoulder: Its treatment by transplantation of the long head of the biceps. Am J Surg 6:815, 1929. 98. Nicola T: Recurrent dislocation of the shoulder. Am J Surg 86:85-91, 1953. 99. Gallie WE, Le Mesurier AB: An operation for the relief of recurring dislocation of the shoulder. Trans Am Surg Assoc 45:392-398, 1927. 100. Helfet AJ: Coracoid transplantation for recurring dislocation of the shoulder. J Bone Joint Surg Br 40:198-202, 1958. 101. Latarjet M: Technic of coracoid preglenoid arthroereisis in the treatment of recurrent dislocation of the shoulder. Lyon Chir 54:604-607, 1958. 102. Eden R: Zur operativen Behandlung der habituellen Schulterluxation unter mitteilung, eines neuen Verfahrens bei abriss am inneren Pfannenrande. Deutsche Z Chir 144:269, 1918. 103. Hybbinette S: De la transplantation d’un fragment osseux pour remedier aux luxations recidivantes de l’epaule; constatations et resultats operatiores. Acta Chir Scand 71: 411-445, 1932. 104. Zuckerman JD, Matsen FA 3rd: Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am 66:175-180, 1984. 105. Bach BR Jr, O’Brien SJ, Warren RF, Leighton M: An unusual neurological complication of the Bristow procedure. A case report. J Bone Joint Surg Am 70:458-460, 1988. 106. Kim SH, Ha KI, Kim SH: Bankart repair in traumatic anterior shoulder instability: Open versus arthroscopic technique. Arthroscopy 18:755-763, 2002.
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107. Cole BJ, L’Insalata J, Irrgang J, Warner JJ: Comparison of arthroscopic and open anterior shoulder stabilization. A two- to six-year follow-up study. J Bone Joint Surg Am 82:1108-1114, 2000. 108. Cole BJ, Warner JJ: Arthroscopic versus open Bankart repair for traumatic anterior shoulder instability. Clin Sports Med 19:19-48, 2000. 109. Green MR, Christensen KP: Arthroscopic versus open Bankart procedures: A comparison of early morbidity and complications. Arthroscopy 9:371-374, 1993. 110. Pagnani MJ, Dome DC: Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am 84:711-715, 2002. 111. Uhorchak JM, Arciero RA, Huggard D, Taylor DC: Recurrent shoulder instability after open reconstruction in athletes involved in collision and contact sports. Am J Sports Med 28:794-799, 2000. 112. Magnusson L, Kartus J, Ejerhed L, et al: Revisiting the open Bankart experience: A four- to nine-year follow-up. Am J Sports Med 30:778-782, 2002. 113. Mohtadi NG, Bitar IJ, Sasyniuk TM, et al: Arthroscopic versus open repair for traumatic anterior shoulder instability: A meta-analysis. Arthroscopy 21:652-658, 2005. 114. Walch G, Boileau P, Levigne C, et al: Arthroscopic stabilization for recurrent anterior shoulder dislocation: Results of 59 cases. Arthroscopy 11:173-179, 1995. 115. Mologne TS, Lapoint JM, Morin WD, et al: Arthroscopic anterior labral reconstruction using a transglenoid suture technique. Results in active-duty military patients. Am J Sports Med 24:268-274, 1996.
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116. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111-122, 1987. 117. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two- to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 118. Potzl W, Witt KA, Hackenberg L, et al: Results of suture anchor repair of anteroinferior shoulder instability: A prospective clinical study of 85 shoulders. J Shoulder Elbow Surg 12:322-326, 2003. 119. Hubbell JD, Ahmad S, Bezenoff LS, et al: Comparison of shoulder stabilization using arthroscopic transglenoid sutures versus open capsulolabral repairs: A 5-year minimum follow-up. Am J Sports Med 32:650-654, 2004. 120. Mazzocca AD, Brown FM,Jr, Carreira DS, et al: Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med 33:52-60, 2005. 121. O’Neill DB: Arthroscopic Bankart repair of anterior detachments of the glenoid labrum. A prospective study. J Bone Joint Surg Am 81:1357-1366, 1999. 122. Stein DA, Jazrawi L, Bartolozzi AR: Arthroscopic stabilization of anterior shoulder instability: A review of the literature. Arthroscopy 18:912-924, 2002. 123. Verma NN, Drakos M, O’Brien SJ: Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy 21:764, 2005.
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CHAPTER 18 Posterior Shoulder Instability John C. Austin, Samer S. Hasan, Timothy P. Heckmann, and Thomas N. Lindenfeld
Posterior instability of the shoulder is less commonly diagnosed than anterior instability of the shoulder. The prevalence of posterior instability is unknown because of a lack of specific diagnostic criteria, but it may affect 5% or more of all patients with glenohumeral instability.1,2 The cause of posterior shoulder instability can be traumatic or atraumatic, or it can arise as a component of multidirectional instability. Patients are most commonly young men between the ages of 15 and 30 years who are frequently involved in overhead or contact sports. Partly because of the difficulty in accurate diagnosis, treatment strategies have varied widely and many open and arthroscopic surgical techniques have been described in the literature.3-7
a primary cause of posterior shoulder instability, although it may be a contributory factor.9,10 In this chapter, the pathoanatomy, description of affected athletes, physical examination, imaging studies, nonoperative management, operative management, and treatment results for posterior shoulder instability will be reviewed.
ANATOMY, BIOMECHANICS, AND PATHOMECHANICS OF POSTERIOR INSTABILITY There are static and dynamic determinants that function to achieve glenohumeral joint stability. Static determinants include glenohumeral joint morphology, the labrum, and capsuloligamentous constraints.
Traumatic posterior shoulder instability frequently involves contact sports such as football or rugby. Other traumatic causes include accidents involving automobiles, all-terrain vehicles, and motocross racing and violent military or labor injuries that often involve catching a heavy load from overhead. The mechanism of injury is frequently an acute posterior force on the glenohumeral joint in a flexed, adducted, and internally rotated position. As a result of the injury, the shoulder may dislocate. The direction of dislocation is typically posteroinferior, in the same manner as the more common anteroinferior dislocation. Traumatic injuries are often associated with a posterior Bankart lesion, with detachment of the posterior capsule and labrum below the glenoid equator, and a stretch injury to the posteroinferior capsule with injury to the posterior band of the inferior glenohumeral ligament. These injuries can be associated with a bony posterior glenoid rim fracture and a reverse Hill-Sachs lesion (Fig. 18-1), which is an anterosuperior humeral head impaction fracture or defect resulting from a posterior dislocation.
The concave shape of the glenoid provides some inherent stability as it articulates with the convex surface of the humeral head. This depth is increased by the glenoid labrum. Concavity compression is an important stabilizing mechanism in which compression of the convex humeral head into the concave glenoid fossa resists humeral head translation. Glenoid version influences glenohumeral stability and varies in the normal population.11,12 Excessive retroversion of the glenoid and loss of concavity of the inferior aspect of the glenoid have been associated with atraumatic posterior shoulder instability.12,13 Glenoid retroversion is infrequently a primary cause of instability,2 but it should be considered as a contributory factor. Kim and colleagues12 have assessed glenoid osseous and chondrolabral retroversion using magnetic resonance arthrography. Osseous and chondrolabral retroversion varies between the superior, middle, and inferior aspects of the glenoid. Furthermore, patients with posteroinferior glenohumeral instability had 4 degrees of increased chondrolabral retroversion in the middle and inferior planes compared with normal controls. Normal chondrolabral glenoid retroversion ranged from 1 to 8 degrees in patients without glenohumeral instability and from 5 to 9 degrees in patients with posteroinferior instability.
Atraumatic posterior shoulder instability can be associated with repetitive microtrauma such as repetitive heavy weightlifting during bench press activities, cumulative injury from push-ups, and sports that demand wide arcs of glenohumeral motion, such as swimming and golf. The follow-through phases of golf and swimming can place significant stress on the posterior shoulder capsule. Atraumatic posterior instability may occur theoretically from excessive humeral head retroversion, posterior glenoid dysplasia, or increased glenoid retroversion. Glenoid dysplasia is rare and is often associated with brachial plexus birth palsy.8 Increased glenoid retroversion is infrequently
Soft tissue structures such as the glenohumeral ligaments and shoulder capsule also contribute to glenohumeral stability. Just as the anterior band of the inferior glenohumeral ligament is an important restraint to anterior humeral head translation in abduction and external rotation, 209
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Figure 18-1. Reverse Hill-Sachs lesion. Note the increased signal on this magnetic resonance imaging scan along the anterosuperior humeral head.
the posterior band of the inferior glenohumeral ligament similarly restricts posterior translation of the humeral head in internal rotation.14 Tears involving the posteroinferior capsulolabral complex, termed a reverse Bankart lesion, often involve the posterior band of the inferior glenohumeral ligament and are frequently associated with a traumatic shoulder injury. Posterior capsulolabral deficiency can also be degenerative in origin, related to repetitive microtrauma or recurrent subluxations.4,6,7 Biomechanical studies have increased our understanding of the pathology associated with posterior shoulder dislocation and subluxation. Recurrent subluxation can create plastic deformation of the posteroinferior capsule, leading to increased joint volume.2 The presence of synovial fluid within a finite volume contributes to articular adhesioncohesion forces and, with negative intra-articular pressure, helps stabilize the glenohumeral joint further.15 These passive restraints become less effective in the presence of increased capsular volume. Other studies have examined capsuloligamentous injury following posterior shoulder dislocation using cadaver models. Warren and associates16 have reported increased posterior translation of the humeral head relative to the glenoid in adduction and internal rotation with sectioning of the posterior band of the inferior glenohumeral ligament and posterior capsule. The rotator interval is the region of the anterosuperior capsule between the superior border of the subscapularis tendon and anterior border of the supraspinatus tendon (anterosuperior capsule from the 12- to 3-o’clock position for a right shoulder). It helps to prevent instability in patients
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with excessive posterior or inferior translation, especially with the arm adducted.17 Warren and coworkers16 have found that the rotator interval has to be sectioned for complete posterior shoulder dislocation to occur. Ovesen and colleagues18,19 have reported that posterior glenohumeral dislocation in a position of adduction and internal rotation creates a posterior capsule injury, along with complete rupture of the teres minor and partial injury of the infraspinatus. There is also injury to the anterior capsule, most notably at the rotator interval. Weber and Caspari20 have studied posterior dislocations in cadavers with the shoulder in forward flexion and internal rotation. Posterior capsulolabral avulsions were found in all specimens tested; it was concluded that injury to the posterior band of the inferior glenohumeral ligament and posterior capsule leads to posterior instability. Collectively, these studies have contributed to the development of the circle concept of shoulder instability, in which increased translation and subluxation are possible with ligament injuries to one side of the joint, whereas complete dislocation requires capsuloligamentous injury on both sides. This has led to the concept of repair of the rotator interval in the treatment of marked posteroinferior glenohumeral instability. Other cadaver studies have examined the material properties of the posterior capsule and the effect of capsulorrhaphy on glenohumeral range of motion. Bey and associates21 have examined the mechanical properties of the posterior glenohumeral capsule and found no significant differences in failure strains or material properties among the superior, middle, and inferior portions of the posterior capsule and the anterior band of the inferior glenohumeral ligament. Mechanical testing has demonstrated that 75% of specimens fail near the glenoid insertion. The posterior strains are highest near the glenoid, which explains why the glenoid labrum and capsule near the glenoid fail more commonly than off the humeral attachment or in the midcapsular region. Gerber and coworkers22 have performed a cadaver study examining the effects of selective capsulorrhaphy on glenohumeral joint passive range of motion. One-centimeter selective capsular plications were performed on eight human cadaver shoulders, with subsequent analysis of shoulder range of motion. Anterosuperior capsular plication (rotator interval closure) decreases external rotation of the adducted arm by 30 degrees. Total posterior capsular plication limits internal rotation by more than 20 degrees. Total inferior capsular plication restricts abduction by a mean of 28 degrees. Another cadaver study23 has examined the effects of arthroscopic thermal capsulorrhaphy of the posterior glenohumeral capsule with a radiofrequency probe. There was no significant decrease in posterior or anterior glenohumeral translation following thermal capsulorrhaphy. It was proposed that the paucity of collagen in the thin posterior capsule explains the ineffectiveness of thermal capsulorrhaphy in this region. Lesions associated with posterior shoulder instability include injuries to the posterior capsule and ligaments,
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labral lesions, chondrolabral lesions, and glenoid defects. Posterior capsuloligamentous disruption can occur at its glenoid or humeral attachment sites, as well as in the midportion of the posterior capsule. Posterior capsuloligamentous disruption at the glenoid attachment site is the most common.6,21,24 Avulsion of the humeral attachment of the posterior capsule and posterior band of the inferior glenohumeral ligament is called a reverse humeral avulsion of the glenohumeral ligament (reverse HAGHL) and is relatively uncommon (Fig.18-2).25-27 There have been case reports of reverse HAGHL lesions caused by sports contact injury and trauma. Posterior midcapsular disruption allows for arthroscopic visualization of the infraspinatus and teres minor and is less common than avulsion from the posterior labrum.28 Rotator interval insufficiency can be associated with injuries to the coracohumeral, superior, and middle glenohumeral ligaments, and may contribute to bidirectional (posterior and inferior) instability.2 Four types of labral lesions have been described— nondisplaced tear, marginal crack (Kim lesion), chondrolabral erosion, or flap tear. The Kim lesion is a superficial crack between the posteroinferior labrum and glenoid articular cartilage.29 This subtle surface change often belies more extensive deep capsuloligamentous stripping. Posterior labral and chondrolabral lesions include posterior chondrolabral defect of the glenoid rim and posterior labrocapsular periosteal sleeve avulsion (reverse anterior labroligamentous periosteal sleeve avulsion [reverse ALPSA] lesion).30 Posterior chondrolabral defects of the glenoid rim are caused by posterior subluxation or dislocation of the humeral head.5,6 A posterior labrocapsular periosteal sleeve avulsion occurs when the posterior labrum is avulsed along
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with a sleeve of adjacent periosteum of the posterior glenoid neck, with subsequent healing of the posterior labrum to the glenoid neck. An osseous defect of the posterior glenoid rim (reverse osseous Bankart lesion) can be associated with posterior shoulder instability.7 One study has found an association between recurrent posteroinferior glenohumeral instability and an osseous defect of the posteroinferior glenoid rim longer than 12 mm.10 Lippitt and Matsen31 have reported a study of ten cadaver shoulders in which all soft tissue had been resected, leaving only the glenoid bone, labrum, and humeral head to provide stability. With a 50-N compressive load, the maximum posterior translation force that can be maintained without posterior humeral head dislocation is 17 N. With 100 N of compression, the maximum posterior translation force is 30 N. This can be expressed as a posterior glenohumeral stability ratio, which is a measure of posterior translation force that can be stabilized under a given compressive load of 30%. The stability ratio following labral excision was reduced by approximately 20%; however, because the study involved older cadavers with relatively atrophic labra, the labrum may provide even greater stability in younger individuals. Concavity compression is hypothesized to be particularly important in the midrange of glenohumeral motion because the capsuloligamentous structures are lax in this position.32
ATHLETE AND PATIENT PRESENTATION Athletes who develop posterior shoulder instability are frequently involved in sports involving strenuous or repetitive upper extremity use, such as football, baseball, swimming, gymnastics, and golf. Athletes may present with a chief complaint of pain, instability, or both. They often present with posterior shoulder pain and may also report involuntary subluxation that affects their athletic performance. This group of patients often has symptoms in only one shoulder.2 Some patients can voluntarily subluxate or dislocate their shoulder in certain positions or have subluxation that is present during the physical examination. Pain or a sensation of instability or subluxation is usually present during axial loading of the humerus in flexion, adduction, and internal rotation.
Figure 18-2. Reverse humeral avulsion of the glenohumeral ligament (reverse HAGHL) lesion. The posterior capsuloligamentous structures have avulsed off of their humeral attachment in this T2-weighted magnetic resonance imaging scan.
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Posterior shoulder instability may be traumatic, atraumatic, or voluntary. Traumatic posterior shoulder instability includes dislocation and subluxation. Recurrent posterior shoulder instability can develop following a posterior shoulder dislocation,3 although this is less common than recurrent anterior instability following an anterior dislocation. Posterior shoulder subluxation often occurs in patients who report a significant injury (“macrotrauma”), such as an
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axial loading injury in internal rotation or a suddenly applied posterior force to the front of the shoulder.6,24,25 Posterior shoulder subluxation, which commonly manifests as pain rather than instability, is common in contact athletes, such as football, lacrosse, and rugby players.33 Although not common in the athletic population, a locked posterior shoulder dislocation (Fig. 18-3) can occur. Patients frequently present with the affected arm in an adducted and internally rotated posture. Posterior shoulder dislocations are associated with seizures (epilepsy), electrocution, and falls sustained by older patients with dementia. A locked posterior shoulder dislocation can be associated with large, engaging reverse Hill-Sachs lesions and reverse Bankart lesions in addition to disruption of the posterior capsulolabral restraints. These injuries can be missed in the emergency room because, unlike an anterior shoulder dislocation, the findings on anteroposterior
radiographs may be subtle. An axillary lateral radiograph will clearly reveal the posterior dislocation (see Fig. 18-3), although obtaining this can be challenging because of patient discomfort. Atraumatic posterior shoulder instability includes patients who develop symptoms insidiously after repetitive minor trauma characterized by a posteriorly directed force applied to the shoulder in a flexed, internally rotated position. Repetitive microtrauma is commonly seen in athletes such as football linebackers and linemen involved in tackling and blocking, bench pressing with heavy weights, and repetitive overhead activities, such as swimming, golf, baseball, tennis, and gymnastics. Hovis and associates34 have described a group of elite golfers who developed posterior instability of the shoulder of the lead arm, which is in the provocative position of adduction and flexion at the top of the back swing. The third group consists of patients who can voluntarily demonstrate posterior shoulder instability in certain provocative positions. Patients with psychological problems may be able to demonstrate voluntary subluxation or dislocation. They often develop instability during adolescence for secondary gain or attention seeking. Some patients can subluxate their shoulder when it is positioned in flexion, adduction, and internal rotation. The shoulder relocates as it is moved into abduction from this position. Positional shoulder subluxation is not usually associated with psychological abnormalities, and these patients generally present with instability rather than pain.
PHYSICAL EXAMINATION A
B Figure 18-3. Locked posterior shoulder dislocation radiographs. A, Anteroposterior view. B, Lateral view. These images reveal humeral head impaction on the posterior glenoid rim. The axillary radiograph clearly reveals the posterior position of the humeral head relative to the glenoid.
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Physical examination begins with a thorough evaluation of all aspects of the shoulder. It is important to establish whether the instability is unidirectional, bidirectional, or multidirectional. The signs of instability are often subtle and nonspecific, and other pathology such as impingement or muscular weakness may also be present. Comparison testing of the affected shoulder with the opposite shoulder is also important. Posterior humeral head translation on the glenoid up to the posterior glenoid rim is common in athletes and may not be pathologic. There is a wide spectrum of symmetrical glenohumeral joint laxity in recreational athletes, and increased shoulder passive range of motion has not been found to correlate with increased glenohumeral joint laxity.35 Provocative testing may help establish the diagnosis by demonstrating asymmetrical and excessive posterior humeral head translation as well as pain, discomfort, or apprehension during testing. Tests include the load and shift test,36 sulcus sign,37 posterior drawer test,38 jerk test,39 and Kim test39 (see Chapter 4). We briefly review a few select tests that we use for patients with posterior instability.
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Gerber and Ganz38 first described the posterior drawer test (Fig. 18-4). The patient is supine with the examiner standing in front of the patient. For examination of the left shoulder, the examiner grasps the proximal forearm with his or her left hand, positions the elbow in 120 degrees of flexion, and positions the shoulder in 80 to 120 degrees of abduction and 20 to 30 degrees of forward flexion. The examiner holds the scapula with her or his right hand, with the index and middle fingers on the scapular spine and thumb immediately lateral to the coracoid process. The examiner then slightly rotates the patient’s upper arm medially and flexes it to about 60 to 80 degrees with the left hand while the examiner’s right hand thumb applies a posterior force to the humeral head. The degree of posterior displacement of the humeral head can be appreciated as the thumb slides along the lateral aspect of the coracoid process while the humeral head contacts the ring finger of the examiner’s right hand posteriorly. Apprehension
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during the application of posterior force is considered to be a positive test for posterior instability. The jerk and Kim tests have been used to assess posteroinferior instability of the shoulder. The jerk test (Fig. 18-5) is performed with the patient sitting. The examiner holds the scapula with one hand, and the patient’s arm is flexed 90 degrees and internally rotated 90 degrees. The elbow is flexed to 90 degrees and a posterior force is then applied with the examiner’s other hand by pushing on the patient’s flexed elbow. The shoulder is then brought into extension beyond the scapular plane. A palpable and often painful audible shift occurs in a positive test as the humeral head
A
A
B B Figure 18-4. Posterior drawer test. A, Starting position. B, Completed position.
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Figure 18-5. Jerk test. A, A posterior force is applied to a flexed, internally rotated shoulder. B, The shoulder is then extended beyond the scapular plane. Anterior humeral head translation and pain during the maneuver is a positive test.
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reduces over the glenoid rim and into the glenoid fossa from a subluxed position.40,41 Pain may or may not be associated with posterior clunking during the jerk test. One study42 has divided patients with posteroinferior shoulder instability into two groups, patients with a painless jerk test and those with a painful jerk test. The group with a painful jerk test had a significantly higher failure rate with 6 months of nonoperative treatment (84% versus 7% failure for the group with a painless jerk test). It was concluded that shoulders with symptomatic posteroinferior instability coupled with a painful jerk test have a high likelihood of a posteroinferior labral lesion requiring arthroscopic repair. The Kim test is performed with the patient sitting with the arm in 90 degrees of abduction. The examiner holds the patient’s elbow and lateral aspect of the proximal arm, and an axial loading force, and 45 degrees of upward diagonal elevation are applied simultaneously. The onset of posterior shoulder pain is defined as a positive test result, regardless of the accompanying clunk of the humeral head. A countersupport, such as the back of a chair or an assistant providing scapular stabilization, is important to allow for application of firm axial compression to the humeral head against a fixed glenoid surface. Kim and coworkers39 have reported that the Kim test is more sensitive in detecting an inferior labral lesion, whereas the jerk test is more sensitive in detecting a posterior labral lesion. One specific type of traumatic posterior instability is the locked posterior dislocation. Patients with a locked posterior shoulder dislocation often present with the shoulder in an adducted, internally rotated position, with loss of external rotation. The coracoid process may be prominent with posterior shoulder fullness.
posterior dislocation (see Fig. 18-3). The anteroposterior radiograph is less reliable for the identification of a posterior dislocation, although it may demonstrate overlap of the medial aspect of the humeral head with the lateral aspect of the glenoid or an incongruent glenohumeral joint space. Computed tomography (CT) is useful for assessment of osseous structures, such as glenoid retroversion and associated glenoid fractures and insufficiency. Humeral head retroversion and reverse Hill-Sachs lesions are also clearly visualized. CT arthrography can assess the glenoid labrum in cases in which magnetic resonance imaging (MRI) cannot be performed for medical reasons (e.g., pacemaker implantation), although CT arthrography now has largely been supplanted by magnetic resonance arthrography. Ultrasound has not been used routinely for the assessment of posterior glenohumeral instability. Borsa and colleagues45 have compared dynamic ultrasound with stress radiographs and found that ultrasound can be a valid and reproducible method for assessing glenohumeral laxity in a clinical setting. Ultrasound, which is cost effective and uses nonionizing radiation, may become a useful tool for evaluating glenohumeral stability in the future. MRI (Fig. 18-6) is the most common method used for shoulder imaging; it is especially useful for imaging soft tissues such as muscle, tendon, labrum, and capsule. MRI also clearly illustrates associated bone marrow edema on T2-weighted imaging. Magnetic resonance arthrography (MRA) involves injection of a contrast agent into the shoulder joint before MRI (Fig.18-7). This is an invasive procedure, but it allows for
IMAGING STUDIES Standard shoulder radiographs are often normal in patients with posterior shoulder instability,24 especially when the cause is atraumatic. Nonetheless, radiographs should be obtained, including true anteroposterior (Grashey view, 30 degrees from the horizontal axis of the body), axillary lateral, and supraspinatus outlet views. Radiographs may demonstrate bony defects of the glenoid and humeral head, especially following acute trauma. The anteroposterior view in external rotation may allow for identification of a reverse Hill-Sachs lesion of the anterosuperior humeral head. The axillary lateral radiograph may demonstrate a reverse bony Bankart lesion. The axillary lateral may also demonstrate calcification along the posterior aspect of the capsule and glenoid labrum. This calcification or exostosis is termed the Bennett lesion43 and is a sign of the presence of posterior instability.44 As shown earlier, the axillary lateral is also useful to rule out a locked
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Figure 18-6. Magnetic resonance imaging scan of posterior labral tear. A gap is clearly visualized between the posterior glenoid and the labrum. Note the slight posterior subluxation of the humeral head.
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Stages of Conservative Rehabilitation Conservative management can be broken up into four phases: (1) acute phase, (2) intermediate phase, (3) advanced strengthening phase, and (4) return to activity. These phases do not have specific timetables, and typically there are no clear-cut demarcations when moving from one phase to the next. The goal of nonoperative rehabilitation is to allow the patient to return to full activity with minimal risk for reinjury. Again, it is important to keep in mind that the program progression is not time based but is based on achieving evaluation goals.
Figure 18-7. Magnetic resonance arthrography scan of posterior capsular laxity. Note the redundant posterior capsule in a patient with posterior glenohumeral subluxation.
superior evaluation of subtle labral tears and joint volume. MRA is currently the best method for imaging capsulolabral disruption46-49; it can visualize posterior labral tears and rotator interval lesions effectively in addition to assessing posterior capsular volume.24 Volpi and associates50 have compared MRI with MRA in 58 patients with glenohumeral joint instability; 11 of 52 labral tears were not recognized before gadolinium contrast injection. Osseous deficiencies can also be visualized, although not as well as with CT.
Phase 1—Acute Phase. Initiation of conservative treatment begins with immobilization after an acute traumatic dislocation. Immobilization begins with the use of an UltraSling (DonJoy, Vista, Calif) positioning the arm in slight abduction and neutral to slight external rotation (Fig. 18-8). The sling is for short-term use to control pain and allow return of active muscle control. Cryotherapy and therapeutic physical therapy modalities are used for pain and swelling management. Pain control is important to allow for early return of muscle function. Passive ROM is initiated, followed by a progression to active ROM as tolerated. Early avoidance of abduction, horizontal adduction, and internal rotation is necessary to protect the posterior structures. ROM exercises include the use of Codman’s exercises, pendulum, pulleys, wand, and gentle external rotation stretching. Progression to strength exercises are also initiated during this phase. These exercises include co-contraction upper extremity shrugs and isometrics for flexion, abduction,
TREATMENT OF POSTERIOR INSTABILITY Nonoperative Management Conservative management for posterior instability is typically the initial treatment of choice. The key to success for this type of treatment lies in the initial accurate diagnosis of the primary injury (e.g., instability) and potential secondary problems (e.g., rotator cuff impingement, scapular dyskinesia). In many cases, glenoid labrum tears are associated with posterior instability. As noted, the skills of the clinician for differential diagnosis are critical. Conservative management requires close communication between the physician and rehabilitation staff. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be necessary to control pain and subacromial swelling. Physical therapy modalities should be used when appropriate. Emphasis on restoring normal function through range-of-motion (ROM) and strength exercises is important. Neuromuscular control by balancing the rotator cuff and the periscapular muscles will assist in controlling overuse injuries. Patient education is important for limiting voluntary subluxation episodes to control joint surface damage.2
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Figure 18-8. Immobilization after acute traumatic dislocation. The arm is positioned in slight abduction and neutral to slight external rotation.
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extension, and external rotation. During this phase, monitoring the return of normal scapulohumeral rhythm can be initiated. Isometric and gentle isotonic scapular retraction exercises can be included. The goals of phase 1 treatment emphasize decreasing pain and inflammation, restoring full, nonpainful ROM, and maintaining active muscle control. Therefore, any activity that reproduces symptoms should be avoided. Phase 2—Intermediate Phase. Progression to this phase occurs when the patient has complete or almost complete ROM, and minimal to no pain. Emphasis shifts to allow for continuing stretching and ROM exercises to restore any ROM not regained with the initial phase of treatment (Fig. 18-9). ROM activity in the elevation planes should be completed in the plane of the scapula. Cryotherapy and other modalities may be used as needed. Strength exercises progress to isotonic exercises with a Thera-Band (Hygenic, Akron, Ohio,) or dumbbell weights. Although dumbbells might be preferred, it may be necessary to use a Thera-Band for the home exercise program. One of the advantages of using dumbbells is the ability to progress the resistance in small, objective increments. Directions of exercise should emphasize flexion, abduction, internal rotation, external rotation (Fig. 18-10), and extension and scapular retraction, protraction, elevation, and depression. However, care is needed to ensure that there is sufficient rotator cuff strength before initiating elevation exercises to avoid impingement. This must be achieved by emphasizing muscular control for the posterior rotator cuff and serratus anterior, which is important because many patients with nontraumatic posterior instability have poor scapular protraction control with elevation. During this phase, eccentric control is emphasized with the use of a Thera-Band for external rotation from neutral rotation to external rotation and return to start position. Neuromuscular control should be initiated with various proprioceptive neuromuscular facilitation (PNF)
Figure 18-10. Thera-Band exercise. This exercise emphasizes external rotation.
Figure 18-9. Stretching and range-of-motion exercises. These exercises are used to restore any range of motion not regained during the initial phase of treatment.
Figure 18-11. Enhancement of the dynamic stability of the glenohumeral joint with the use of proprioceptive neuromuscular facilitation techniques.
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techniques.51 These are designed to enhance the dynamic stability of the glenohumeral joint as the patient is progressed into the later stages of rehabilitation (Fig. 18-11). Diagonal patterns for strengthening using a Thera-Band represent an excellent method for control during the home exercise program. Goals of this phase allow for regaining and improving muscular strength and improving neuromuscular control. Rotator cuff control dictates this progression. Dumbbell progression goals for side-lying external rotation and internal rotation (Table 18-1) are 10 and 15 pounds, respectively, and 15 to 25 pounds for shoulder shrugs.
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TABLE 18-1 Dumbbell Progression Goals Athlete External Rotation (lb)
Internal Rotation (lb)
Female
7-8
10-12
Male
8-10
12-15
Phase 3—Advanced Strengthening Phase. Isotonic exercise is continued, with an emphasis on rotator cuff and scapular muscle strengthening. Emphasis should be placed on proper technique and on sufficient sets and repetitions to allow for achieving muscle fatigue. When dealing with an athletic population, isokinetic exercise programs can be used. A velocity spectrum program at moderate to high speeds (180 to 300 deg/sec) can be used to allow for accommodating resistance programs. Seated external and modified internal rotation in the scapular plane with the arm at the side is the initial position for strength training. Plyometric exercises are used to allow for functional progression in an attempt to return an athlete to his or her sport. Initially, the TheraBand is used and then progressed to include medicine balls, wall push-ups (Fig. 18-12), and reverse wall push-ups. Care must be taken regarding strenuous exercises that could stress the posterior capsule. For example, this would relate to using the wall push-up to strengthen the serratus anterior while potentially stressing the posterior aspect of the shoulder (Fig. 18-13). Goals of this program include increasing strength, power, and endurance to within normal limits and preparing the athlete for return to activity. Phase 4—Return to Activity. Transition into this phase requires continuation of the prior exercise program to allow full return of strength. Evaluation must be a key to
Figure 18-13. Use of the wall push-up to strengthen the serratus anterior while stressing the posterior aspect of the shoulder.
this transition. Pain, ROM, strength, and tolerance for activities of daily living (ADLs) should all be considered. Typically, this is the preparation phase for resuming full activity. Strength and plyometric exercises attempt replication of functional sports movement. In addition, performing sport-specific tasks are included. If overhead throwers are used as an example, an interval throwing program would be initiated during this phase. Progression of throwing uses a warm-up, short toss–long toss; pitchers throw from the level surface and advance to the mound, and eventually progress to game simulation. This progression is predicated on using evaluation as the basis for program advancement. Because of the posterior instability, care should be observed during the pullthrough phases of swimming and rowing, swinging a bat, and overhead sports. Goals of this program allow for full return to sports or activity.
Operative Management
Figure 18-12. Plyometric exercise, such as wall push-ups, are used to allow for functional progression back into sports.
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Many have suggested that surgical treatment of posterior shoulder instability may be considered after failure of conservative treatment that has consisted of an initial trial of physical therapy for 6 months.1,4,6 The senior author (TNL) does not set arbitrary limits on time before recommending surgical intervention. If, by isokinetic testing, the patient can objectively demonstrate full rehabilitation of the rotator cuff, no further improvement in symptoms are likely to be achieved with continued physical therapy. Surgery may be indicated at this time. Furthermore, if the patient
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appears genuinely motivated to participate fully in a physical therapy program, but these efforts cannot continue because of pain or repeated episodes of instability, a decision to proceed with surgery may be reasonable. Operative treatment aimed at repairing structural damage may be offered at an earlier stage to select patients, such as collision athletes with traumatic posterior instability and a posterior labral tear.2 Factors favoring acute repair include age younger than 30 years, trauma with significant force in a patient without a history of shoulder subluxations, dominant arm, high present activity level with a desire to continue a high level of activities, or a sensation of instability while the arm is in the sling or with minimal arm movement.52 Timing of surgery for athletes should correspond to the patient’s specific situation. Surgery should be coordinated to minimize the risk of further injury while optimizing the patient’s participation in future athletic endeavors. Most lesions associated with posterior instability can be treated arthroscopically, although some situations may demand open intervention. In all cases, surgery begins with an examination under anesthesia and careful, systematic diagnostic arthroscopy. Examination under anesthesia allows for comparison of findings present during physical examination in the awake patient and provides a final confirmation of the pathology before surgical treatment. Both shoulders should be examined for side-to-side comparison. The patient can be positioned in the beach chair or lateral decubitus position. The lateral decubitus position may allow for better exposure to the inferior capsule and inferior labrum because of the enhanced ability to distract the glenohumeral joint. Diagnostic arthroscopy can be performed to confirm findings seen on MRI or MRA, assess for additional pathology that may be contributing to the instability, and verify the appropriateness of arthroscopic versus open repair. Following the examination under anesthesia, the patient is turned into the lateral decubitus position (Fig. 18-14). The arm is placed in approximately 30 degrees of abduction and 20 degrees of flexion with a pulley system with approximately 10 pounds of weight used to suspend the arm. The amount of weight used is adjusted appropriately according to the patient’s size. The arthroscope is inserted into the posterior portal first and the articular surfaces of the glenoid and humeral head are assessed, as well as the attachment of the rotator cuff tendons. The biceps anchor and superior labrum are visualized, followed by the anterior labrum, anterior capsuloligamentous structures, and axillary pouch. An anterior superior portal is created with a spinal needle entering through the rotator interval. The arthroscope is then moved using a switching stick from the posterior to the anterior portal and the entire posterior and inferior labrum and capsule are carefully inspected and probed. A diagnostic arthroscopy before repair of the injured structures allows for verification of suspected pathology and for assessment of additional pathologic lesions.53
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Figure 18-14. Lateral decubitus position. Note that the arm is in a position of abduction, with slight forward flexion, with the pulley system attached to the contralateral side of the operating table.
Excessive posterior inferior capsular laxity is often observed arthroscopically in patients with posterior shoulder instability. The posterior capsule forms a large pouch in the posterior aspect of the joint, and the entire posterior glenoid rim and labrum can often be viewed from the posterior portal when the tip of the arthroscope is pulled back to the capsule. This unusual view has been termed the skybox view1 (Fig. 18-15). Open Management Posterior capsulolabral plication can be successfully performed arthroscopically, but there are indications for open repair. These include cases of significant posterior glenoid bone loss or a large, engaging reverse Hill-Sachs lesion such as that which might occur with a locked posterior dislocation. Revision surgery for capsuloligamentous
Figure 18-15. Skybox view. The arthroscope is in the posterior portal, demonstrating a patulous posterior capsule with visualization of the posterior labrum.
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deficiency caused by thermal necrosis from prior thermal capsulorrhaphy may require an open approach for reconstruction of the capsuloligamentous structures with allograft or autograft. Open treatment is typically performed via a posterior approach (Fig. 18-16). The patient can be placed in the lateral decubitus or beach chair position as long as a positioner is used that allows for adequate exposure of the posterior shoulder. The skin incision begins 2 cm medially to the posterolateral corner of the acromion and extends 8 cm
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inferiorly toward the posterior axillary crease. The deltoid muscle is then split along its raphe between the middle and posterior thirds. If adequate exposure is not obtained through the deltoid split, the deltoid can be partially detached from the scapular spine and posterior acromion to improve visualization of the posterior aspect of the rotator cuff. There are two approaches through the posterior aspect of the rotator cuff. First, the transverse interval between the infraspinatus and teres minor is developed. Note that this interval is more easily appreciated with medial dissection and identification of the separate muscle bellies because the infraspinatus and teres minor tendons merge together at their lateral insertion on the humerus. Care is taken to protect the suprascapular nerve with medial dissection. Alternately, the infraspinatus tendon is split horizontally in line with its muscle fibers. The infraspinatus muscle is bipennate and inserts onto a broad facet along the posterior aspect of the greater tuberosity, which helps differentiate it from the teres minor. The infraspinatus tendon may be incised vertically at its humeral insertion if additional exposure of the posterior shoulder capsule is required. Care is taken to separate the interval between the rotator cuff tendons and posterior capsule. The infraspinatus tendon is retracted superiorly and the teres minor tendon is retracted inferiorly.
A
B Figure 18-16. Open posterior approach to the glenohumeral joint. A, The deltoid is split along its raphe between the middle and posterior thirds. It can be partially detached along the scapular spine for 1 to 2 cm if improved visualization is required. B, The interval between the infraspinatus and teres minor is developed, and the posterior capsule is exposed. Care is taken to protect the axillary nerve inferior to the teres minor and the suprascapular nerve medially. (From Miller S, Flatow EL: Posterior and Multidirectional Instability: Open Solutions. In Warner JP, Iannotti JP, Flatow EL (eds): Complex and Revision Problems in Shoulder Surgery, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 80-81.)
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The capsule is then incised in a craniocaudal direction 1 cm medially to its insertion on the humerus, starting superiorly and carefully proceeding inferiorly. The capsule is split in a T fashion transversely from the middle of the glenoid to the middle of the humeral head articular surface. The plane between the capsule and the teres minor is bluntly developed, and the axillary nerve is identified and protected. The axillary nerve and posterior circumflex humeral artery reside in the quadrangular space just inferior to the teres minor. The borders of the quadrangular space are the teres minor superiorly, teres major inferiorly, long head of the triceps medially, and humeral shaft laterally. The capsule is dissected off the humeral neck as far inferiorly as is necessary to allow for adequate capsulorrhaphy of the posterior or posteroinferior capsule. The surgeon places an index finger into the axillary pouch to determine the appropriate amount of capsular mobility. Adequate mobilization has been achieved when the surgeon’s finger is extruded by pulling superiorly on capsular traction sutures. The posterior labrum is inspected and repaired, if necessary. When there is a large redundant capsule, the superior capsular flap is shifted inferiorly and secured with nonabsorbable braided sutures; the inferior capsular flap is shifted superiorly in a similar manner. The arm is positioned in 10 degrees of external rotation, 15 degrees of abduction, and 0 degrees of flexion while the capsular flaps are secured. The infraspinatus tendon is repaired (if necessary) with no. 2 braided nonabsorbable suture anchors, and the split in the posterolateral deltoid raphe is repaired. The skin incision is closed with an absorbable subcuticular suture.5
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Correction of osseous anatomy in posterior shoulder instability is infrequently performed. Excessive glenoid retroversion has been treated with posterior glenoplasty, consisting of a posterior opening wedge osteotomy of the glenoid neck with bone graft interposition.9 Posterior bone block glenoid augmentation has been described as primary treatment for patients with deficiency of the posterior lip of the glenoid.54 This is also used in the revision setting in the presence of distorted osseous anatomy. Metcalf and colleagues55 have described the surgical technique for posteroinferior glenoplasty. The glenoid osteotomy is performed 1 cm medial to the posteroinferior glenoid rim. A 2.5-cm osteotome is inserted starting posteroinferiorly and aiming anterosuperiorly for a distance of one half the anteroposterior diameter of the glenoid. The osteotome is carefully wedged open, and a bone graft wedge with a 5-mm base taken from the posterior acromion is carefully impacted into the osteotomy site. It has been demonstrated that posteroinferior glenoplasty increases the tangential force necessary to produce a posteroinferior glenohumeral dislocation under a 50-N compressive load by 70%. These procedures are challenging and should not be performed by the inexperienced shoulder surgeon. The techniques should be practiced first on a cadaver to understand better the three-dimensional glenoid anatomy, especially when approached posteriorly. Arthroscopic Management Arthroscopic treatment of posterior shoulder instability has the advantages of smaller incisions, decreased postoperative pain, and better visualization of capsular and intraarticular anatomy and associated pathology compared with the open approach. Concomitant impingement, acromioclavicular arthrosis, rotator cuff tears, biceps tendon injury, anterior labral tears, and superior labral anteriorposterior (SLAP) tears can be addressed arthroscopically with subacromial decompression, distal clavicle excision, rotator cuff repair, biceps tenodesis or tenotomy, anterior labral repair, or SLAP repair, respectively. Posterior stabilization can be technically challenging because posterior instability is less common than its anterior counterpart. Patients with unidirectional posterior instability and associated capsulolabral lesions have been effectively treated arthroscopically.6,24,56 First, an examination under anesthesia is performed by maintaining scapular stability with one hand and performing humeral head translation with the other hand. The patient is then placed in the lateral decubitus position on the beanbag, as described earlier. Exposure can be enhanced by applying an overhead traction sleeve for abduction, but this may only be needed during the repair process and does not need to be applied during diagnostic arthroscopy or during lesion preparation before repair. A diagnostic shoulder arthroscopy is carried out with the arthroscope in the posterior portal. The skybox view1 is usually noted because of the enlarged posterior capsule
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(see Fig. 18-15). The arthroscope is then transferred to the anterior portal via switching sticks, and the posterior labrum and capsuloligamentous structures are carefully assessed. When a labral detachment is identified, a capsulolabral repair is carried out, whereby a glenoid-based capsular shift is included in the labral reattachment. If the labrum is still attached to the glenoid, a capsular plication is carried out using suture anchors, sutures passed through the intact labrum, or some combination of both. When a posteroinferior labral tear is identified, it is freed from the scapular neck using an arthroscopic elevator. The underlying bone is abraded with a mechanical shaver or small burr, and the capsule and posterior band of the inferior glenohumeral ligament are abraded with an arthroscopic rasp or mechanical shaver, such as a whisker shaver. An accessory posterolateral portal is created about 2 cm inferior and 1 cm lateral to the posterolateral corner of the acromion to assist with suture anchor placement (7-o’clock portal). An inside-out or outside-in technique may be used for placement of the accessory portal. In the inside-out technique, a switching stick or Wissinger rod is placed in the anterosuperior portal and out the posteroinferior capsule. This portal can then be enlarged using dilators. A spinal needle can identify the ideal angle of entry to optimize placement of the accessory posterolateral portal when using the outside-in technique. Care must be taken to avoid placement of the low portal more than 3 cm distal to the acromion to protect the axillary nerve. Other options for portals include using two anterior portals so that the accessory anterior portal is used instead of a second posterior portal for suture management. However, using one posterior portal requires that this portal have an adequate trajectory for appropriate anchor placement and suture passage. Bioabsorbable suture anchors loaded with no. 2 braided nonabsorbable sutures are then placed (Fig. 18-17) and the labrum is repaired (Fig. 18-18) to its anatomic location along the posterior edge of the glenoid rim articular surface. The suture anchors should be on the glenoid face and not medially along the glenoid neck. An appropriate angle of insertion is necessary to avoid damage to the more central aspect of the glenoid articular cartilage as the anchor is inserted. If the posterior capsule is redundant, a capsular plication (Fig. 18-19) may be performed using a Bird Beak suture retriever (Arthrex, Naples, Fla) or a shuttle technique to pass labral sutures. The posteroinferior capsule is shifted superiorly, plicated, and included in the labral repair. A 45-degree curved suture hook, such as the Linvatec Spectrum (ConMed Linvatec, Largo, Fla), is used to pass a no. 1 monofilament suture such as a polydioxanone suture (PDS) through the capsule and then the labrum. The amount of capsule incorporated is proportional to the amount of excess capsular volume. The capsule is first
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Figure 18-17. Suture anchor placement for labral repair. Note that the cannula is kept close to the suture anchor to avoid entangling the sutures in the adjacent soft tissues.
221
Figure 18-19. Posteroinferior capsular plication. A curved shuttle device loaded with monofilament suture is used to capture the posterior capsule inferior to the entrance point in the posterior labrum.
through the suture anchor eyelet. Sliding locking knots are attractive but less forgiving. All knot tying needs to be mastered outside the operating room. Suture anchors and capsular plication proceed in a posteroinferior to posterosuperior direction.
punctured with the curved suture hook inferior to the suture anchor and the second puncture, which includes the labrum, is made more superiorly near the suture anchor. This creates a superior capsular shift along with posterior capsular tightening and advances the posterior band of the inferior glenohumeral ligament. The nonabsorbable suture attached to the anchors is then shuttled through the capsular tissue via the monofilament suture.
The rotator interval capsule should be assessed between the superior aspect of the subscapularis and anterior aspect of the supraspinatus. The rotator interval, which includes the superior and middle glenohumeral ligaments, may be stretched or injured in patients with multidirectional instability.2 If persistent posteroinferior laxity or excessive external rotation, or both, is still present following posterior capsulolabral plication, rotator interval closure (Fig. 18-20) may be performed. Rotator interval closure has been shown to reduce posteroinferior humeral head translation in the adducted position,17 and can be accomplished with the placement of one suture adjacent to the glenoid rim. Additional sutures placed in the rotator interval can lead to overtightening and loss of external rotation.57 The rotator interval capsule tissue is plicated with the patient’s arm in 30 degrees of external rotation; the supraspinatus and subscapularis tendons should not be included in the repair.53 Rotator interval closure may be performed via the anterior cannula with an inside-out technique. With the arm held in 30 degrees of external rotation, the suture is tied over the anterior capsule, with the anterior cannula partially retracted. This can be accomplished without direct visualization or by direct visualization within the subacromial space.
Sutures that slide freely through the anchor eyelet are then tied with a sliding knot, followed by three alternating halfhitches. Surgeons performing arthroscopic repairs should be familiar with sliding and nonsliding knots. Nonsliding knots are required when the suture does not slide freely
Patients with a Kim lesion, an incomplete and concealed avulsion of the posteroinferior labrum (Fig. 18-21), are treated by completing the partial tear with subsequent labral repair, along with repair of the posterior band of the inferior glenohumeral ligament via suture anchors.29
Figure 18-18. Labral repair with suture anchors. The imbricated capsular tissue forms a bumper adjacent to the posterior labrum.
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A Figure 18-21. Kim lesion of posteroinferior labrum.
POSTOPERATIVE REHABILITATION
B Figure 18-20. Rotator interval closure. A single suture is tied in the rotator interval superior to the subscapularis and anterior to the supraspinatus tendons. A, Prerepair. The subscapularis tendon is running in a vertical direction with the widened rotator interval located superiorly (to the right of the subscapularis in the picture). B, Postrepair. Note the decreased space superior to the subscapularis tendon.
Patients with Kim lesions are repaired in the same fashion as those with complete posterior labral tears. The key is to recognize the Kim lesion as a posterior labral tear. This lesion must be fully released from its partially healed position so that the posterior labrum may be advanced and secured to its anatomic location. In patients without labral tears but with posterior capsuloligamentous deficiency, the 45-degree suture hook with monofilament suture is again used to plicate the posterior capsule and repair the posterior band of the inferior glenohumeral ligament to the intact labrum following abrasion of the soft tissues with an arthroscopic rasp. Nonabsorbable sutures are shuttled in a similar fashion via the monofilament suture and are subsequently tied.
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Postoperative rehabilitation is critical to the success of the surgical procedure. Rehabilitation is initiated within the first 2 days postoperatively and is progressed based on the healing principles of the tissues involved, as well as constant re-evaluation of the patient to determine his or her symptomatic progression related to pain, ROM, and strength. It is anticipated that the rehabilitation period will last approximately 6 months, with ROM goals being achieved by approximately 2 to 3 months postoperatively and strength goals by 4 to 5 months. Soft tissue strength may take 6 months or longer to achieve. This is related to the level of postoperative activity the patient desires, as well as any potential postoperative complications.
Acute Phase of Physical Therapy Postoperative immobilization is used to protect the repair. A sling with an abduction pillow is measured and fit to the patient with the arm slightly abducted by the sling’s pillow, and maintained in approximately 15 degrees of external rotation. The sling is removed to permit exercise, icing, and showering. Otherwise, the sling is used for the first 4 to 6 weeks postoperatively. The patient is also encouraged to avoid active internal rotation and horizontal adduction for the initial 4-week postoperative period.59 Within the first 2 days after surgery, active-assisted ROM for the hand, elbow, and neck are initiated. By the end of the first week, active-assisted abduction and external rotation are initiated. Early muscle activation is permitted through submaximal isometric contraction for abduction, adduction, flexion, and extension during the first 1 to 2 weeks. Care must be taken to use pain as a guideline, especially with the elevation planes of movement. ROM goals by the end of the first
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4 weeks are 90 degrees of abduction and 90 degrees of external rotation.59 The sling is normally discontinued after 4 to 6 weeks. Cryotherapy and other physical therapy modalities such as electrical stimulation are encouraged to help control the postoperative pain and inflammation. Arthroscopic intervention may create some slight modifications to the postoperative rehabilitation program. Studies have recommended the use of sling immobilization for approximately 3 to 4 weeks; ROM activities begin at this time. This program uses passive- and active-assisted ROM exercises, such as Codman’s, pendulum, scapular control, and elbow and wrist exercises.6,7,34
Intermediate Phase of Physical Therapy ROM and strengthening are advanced as protective range limitations are slowly lifted. Overhead pulleys are started for forward flexion and abduction. The L bar is also permitted for overhead elevation and external rotation.59 External rotation motion is advanced to include the 0-degree abducted position in the plane of the scapula as well as the 45- and 90-degree abducted positions. Active internal rotation begins with the arm at the side, resting on a towel roll in the gravity neutral position, and is gradually progressed to the antigravity position. At this stage, internal rotation should be attained to approximately 80% of that of the contralateral side.27 Progressive resisted exercises (PREs) are initiated for external rotation, flexion, and abduction.59 In open repairs where the infraspinatus muscle has been detached, external rotation PREs must progress cautiously. Scapular control is also emphasized for protraction, retraction, elevation, and depression. Posterior rotator cuff and scapular control must be emphasized before deltoid control to prevent early overuse injuries. During this phase of rehabilitation, early dynamic control can be enhanced through various PNF procedures. Manual techniques, such as rhythmic stabilization, and equipment techniques, such as the Bodyblade (Hymanson, Playa del Ray, Calif; Fig. 18-22) and Therabar (Hygenic, Akron, Ohio), are designed to produce coordinated muscle effort. Cryotherapy is encouraged after exercising, and modalities are used as needed. This phase of rehabilitation after arthroscopic intervention has a primary focus of initiating a full ROM program to achieve full functional mobility. It includes early work on internal rotation and horizontal adduction. A progressive strength program uses a Thera-Band and PREs. Strength exercises emphasize rotator cuff and scapular stabilizing muscles.6,7,34
Advanced Strengthening Phase During this phase, ROM should be returning to full. Emphasis is placed on progressing muscle strength and dynamic control. Attempts to control the force couples
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Figure 18-22. Demonstration of rhythmic stabilization using the Bodyblade.
between the rotator cuff and scapular stabilizing muscles are initiated. A Thera-Band can be used for early muscle control but, as strength is progressed, a shift in emphasis is placed on dumbbells and free weights. This provides the potential for an objective approach to increasing muscle strength. External rotation at 0 (Fig. 18-23A) and 90 degrees (see Fig 18-23B), internal rotation, scapular retraction, scapular elevation, scapular protraction, horizontal abduction (Fig.18-24), and shoulder extension provide the early key planes for strength. Surgical tubing and a TheraBand are used for eccentric control for external rotation59 (Fig. 18-25). By 12 to 16 weeks postoperatively, it is generally safe to add light horizontal adduction stretching (Fig.18-26) to the program. As long as the program is supervised, a full free weight program can be undertaken. Focus is placed on maximal muscle strengthening and dynamic control. Goals of this phase include asymptomatic ADL activity, full return of muscle strength, and initiating early functional activity for returns to sports or work. By this time after surgery, there is little difference between open and arthroscopic postoperative rehabilitation. The primary focus is on muscle strengthening and controlled sport-specific training. Aggressive strength training may begin if manual muscle testing reaches grade 4⫹ to 5. For activities such as golf, permission for putting and chipping may be given.34 However, protection for overhead and contact activity is still important.6
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A
Figure 18-25. Demonstration of Thera-Band exercise for eccentric control for external rotation.
B Figure 18-23. External rotation. A, Demonstrated at 0 degrees. B, Demonstrated at 90 degrees.
Figure 18-26. Light horizontal adduction stretching.
Figure 18-24. Horizontal abduction. This exercise is an early key plane for strength.
Return to Activity Phase In an athletic population, isokinetic testing would be initiated at approximately 16 weeks postoperatively. The results of the test will dictate the rate of return to activity progression. The patient’s progression from weight training to
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plyometric training using the Plyoback (Exertools, Novato, Calif) and medicine balls (Fig. 18-27) permits advanced strength and function training.59 Isokinetic testing would be used at approximately 4-week intervals to allow for a continued progression of the exercise program. After achieving approximately 80% on bilateral comparisons of the isokinetic data, the patient is permitted to begin the sport-specific training. This level of training typically will occur during postoperative months 4 to 6. Exercise programs at an advanced level continue until the goals for strength and return to the desired activity are achieved. Most patients return to full activity between 6 and 12 months postoperatively.27,58,59
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225
OUTCOMES Open Procedures
A
There have been several studies reporting on the outcomes following open and arthroscopic posterior capsulolabral repair. Studies frequently report on different and often heterogeneous populations, such as patients with traumatic, atraumatic, and volitional causes; many include patients who underwent additional procedures, such as anterior capsulolabral and SLAP repair. Posterior shoulder instability can be difficult to diagnose because of a continuum of pathology, ranging from unidirectional posterior shoulder instability to multidirectional instability with a primary posterior component. The importance of distinguishing patients with acute, traumatic posterior shoulder dislocations from those with recurrent, atraumatic instability has been pointed out.2,24,60 As noted, the former condition results from an isolated traumatic event, whereas the latter condition is related to repetitive microtrauma— repetitive stress to the posterior capsule over time.
Open Treatment
B
C Figure 18-27. Advanced strength and function training using the Plyoback and medicine balls. The rotator cuff and periscapular muscles must work in concert to throw (A, C) and catch (B) at varying trajectories and velocities.
Isokinetic testing following arthroscopic reconstruction begins at approximately 4 months after surgery. This testing represents an important component for activity progression. Goals for return to activity are at 4 to 6 months postoperatively,6 with contact activity protected for a minimum of 6 months.7 Precautions for return to overhead activity require a good maintenance exercise program to control the risk for overuse injuries.
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Hawkins and associates60 first reported on open treatment of posterior shoulder subluxations. Their study reported a high failure and complication rate in 26 shoulders treated with three different surgical techniques—17 glenoid osteotomies, 6 reverse Putti-Platt capsular plications, and 3 biceps tendon transfers. The overall recurrence rate was 50%. Bigliani and coworkers61 have evaluated 35 shoulders in 34 patients treated with open posteroinferior capsular shift; 11 shoulders had prior operations. The patient population was mixed, with 6 shoulders with posterior instability, 7 shoulders with posteroinferior instability, and 22 shoulders with multidirectional instability, posterior and inferior dislocation along with anterior subluxation. Capsular redundancy was found intraoperatively, with only 4 shoulders with complete posterior labral detachment. Subjective patient assessment at a mean 5-year follow-up revealed 80% excellent or good results. Of the fair or poor results, 6 of 7 were in revision cases. Fuchs and colleagues58 have reported on 26 shoulders that underwent open posteroinferior capsular shift; these patients had recurrent, voluntary posterior shoulder subluxation. The mean follow-up period was 7.5 years. All patients failed at least 3 months of physical therapy before operative treatment. Posterior labral repairs were performed in 7 shoulders, 1 shoulder underwent a posterior bone block, and 3 shoulders had a posterior glenoid osteotomy for excessive glenoid retroversion. Recurrent instability developed in 6 of 26 patients (23%); three of these were primary procedures and three were revisions. The clinicians concluded that their intermediate-term results were satisfactory. Recurrence was associated with a prior operation on the
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posterior shoulder or a new traumatic injury. Prevalence of recurrent posterior shoulder instability did not increase over time.
Arthroscopic Procedures Wolf and Eakin1 have studied 14 patients with recurrent posterior shoulder instability treated arthroscopically with a minimum 2-year follow-up. Posterior capsule laxity was present in all cases, and labral pathology was present in 12 patients (86%). Reverse Bankart lesions were seen in 8 of 14 patients (57%). Subjective patient evaluation revealed 12 excellent and 2 fair results; 9 of 10 patients reported full return to preinjury level of function in their respective sport. There was one recurrence, which was treated with a second arthroscopic capsular plication. Antonio and associates4 have evaluated 41 patients with posteroinferior shoulder instability treated with arthroscopic posteroinferior capsular shift, with a mean follow-up of longer than 2 years. Of these patients, 78% reported a traumatic injury; 32 patients had a primary procedure and 9 patients underwent a revision procedure. The patient population consisted of athletes and laborers. No postoperative instability was reported by 59% of patients; 85% of patients noted improved shoulder stability postoperatively based on self-assessment of shoulder function and general health status. Only 2 of the 9 patients who underwent a revision procedure noted no postoperative instability; 19 patients were receiving workers’ compensation, and they showed no statistically significant improvement. Abrams and coworkers53 have studied 48 patients with posterior and posteroinferior instability treated with arthroscopic repair. Posterior labral lesions were noted in 26 patients; 13 patients had anterior labral tears and 4 had SLAP lesions. The series included 26 athletes and 7 workers’ compensation patients. At a mean follow-up of 2 years, they reported a 4% rate of recurrent instability (2 of 48 patients). Four patients had a stable shoulder with residual pain, and 2 patients developed postoperative stiffness that resolved over 6 months. The rate of return to competitive athletics was 85% (22 of 26 athletes). Williams and colleagues7 have conducted a retrospective review of 27 shoulders (26 patients) who underwent arthroscopic posterior Bankart repair, with an average 5-year follow-up. There were no patients with ROM deficits, and 92% of patients were stable at follow-up. Kim and associates6 have reported on 27 patients with traumatic unidirectional recurrent posterior subluxation treated with arthroscopic labral repair along with posterior capsular shift. Patients were evaluated at more than 3 years postoperatively. All patients had a posteroinferior labral lesion, 96% of the shoulders were stable postoperatively, and there were no operative complications. The clinicians concluded that arthroscopic posterior labral repair with
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posterior capsulorrhaphy is an effective treatment for traumatic unidirectional recurrent posterior subluxation, providing stability, pain relief, and functional restoration. Bottoni and coworkers62 have reported on 31 shoulders in 30 patients, with 40-month follow-up, who underwent arthroscopic or open treatment of posterior shoulder instability; 19 patients were treated arthroscopically and 12 were treated via an open posterior approach. Superior outcomes were noted following arthroscopic repair using both the Western Ontario shoulder stability index and the Rowe score. Provencher and colleagues24 have studied 33 patients with posterior shoulder instability who underwent arthroscopic treatment, with a mean follow-up of more than 3 years. Labral repairs were performed in 17 patients, and capsular plication alone was performed in another 16 patients. The rotator interval was closed in 2 of the 33 patients. Thirty patients recalled a traumatic event, and 3 others sustained repetitive microtrauma. Stability was successfully restored in 88% of patients; 7 patients were defined as failures, 4 for recurrent instability and 3 for persistent pain. Patients with voluntary instability and those with prior shoulder surgery demonstrated worse outcomes; 3 of 4 patients who underwent prior thermal capsulorrhaphy were failures. Chhabra and associates56 have recently reported on the largest series of patients undergoing operative posterior shoulder stabilization. They studied 100 overhead and contact athletes with posterior inferior instability who underwent posteroinferior capsulolabral repair using suture anchors without rotator interval closure. Of these athletes, 95% had stable shoulders at a mean follow-up of 2 years postoperatively, and 83% returned to the same level of sport. Other studies have incorporated methods aimed at improving arthroscopic management of posterior shoulder instability. These include various techniques for capsulolabral repair, rotator interval closure, placement of accessory posterior portals, and closure of the capsule defect created by the posterior portal. Different arthroscopic techniques have been described to improve repair of the inferior glenohumeral ligament with capsulolabral plication.63,64 Appropriate placement of accessory posterior portals may allow for improved posteroinferior capsulolabral repair.24,65 Arthroscopic posterior portal closure has been described,66 although it is not done routinely. The significance of holes created by cannulas in the posterior capsule is currently unknown.
SUMMARY Posterior shoulder instability is becoming a more common clinical entity as diagnosis and recognition improve. Most patients with recurrent posterior shoulder instability experience a decrease or resolution of their symptoms following
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physical therapy, which is the initial treatment of choice. Operative intervention is indicated only for certain cases of traumatic instability and when symptomatic involuntary instability or pain persists despite appropriate physical therapy, such as strengthening and neuromuscular conditioning. Operative results of treatment of posterior shoulder instability are initially less favorable than results for anterior shoulder instability. More recently, appropriate recognition and subsequent treatment of specific lesions leading to correction of all components of posterior instability have improved results. Outcomes following arthroscopic treatment are improving over time as techniques evolve. Lesions associated with posterior instability that can be surgically addressed include labral tears, increased posterior capsular volume, a widened rotator interval, and osseous deformity (reverse bony Bankart or large reverse Hill Sachs defect). The best outcomes to date following an open or arthroscopic soft tissue repair have consisted of anatomic restoration of appropriate posteroinferior capsulolabral tension, along with repair of posterior labral pathology. Complex posteroinferior or multidirectional instability patterns may also require plication of the anterior and inferior parts of the capsule and rotator interval closure. Osseous reconstructive procedures are reserved for the rare unstable shoulder with marked glenoid erosion or glenoid retroversion.
References 1. Wolf EM, Eakin CL: Arthroscopic capsular plication for posterior shoulder instability. Arthroscopy 14:153-163, 1998. 2. Robinson CM, Aderinto J: Recurrent posterior shoulder instability. J Bone Joint Surg Am 87:883-892, 2005. 3. McIntyre LF, Caspari RB, Savoie FH 3rd: The arthroscopic treatment of posterior shoulder instability: Two-year results of a multiple suture technique. Arthroscopy 13:426-432, 1997. 4. Antoniou J, Duckworth DT, Harryman DT 2nd: Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am 82:1220-1230, 2000. 5. Pollock RG, Owens JM, Flatow EL, Bigliani LU: Operative results of the inferior capsular shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am 82:919-928, 2000. 6. Kim SH, Ha KI, Park JH, et al: Arthroscopic posterior labral repair and capsular shift for traumatic unidirectional recurrent posterior subluxation of the shoulder. J Bone Joint Surg Am 85:1479-1587, 2003. 7. Williams RJ 3rd, Strickland S, Cohen M, et al: Arthroscopic repair for traumatic posterior shoulder instability. Am J Sports Med 31:203-209, 2003. 8. Waters PM, Bae DS: Effect of tendon transfers and extraarticular soft-tissue balancing on glenohumeral development in brachial plexus birth palsy. J Bone Joint Surg Am 87:320-325, 2005. 9. Wirth MA, Seltzer DG, Rockwood CA Jr: Recurrent posterior glenohumeral dislocation associated with increased retroversion of the glenoid. A case report. Clin Orthop Relat Res (308):98-101, 1994. 10. Weishaupt D, Zanetti M, Nyffeler RW, et al: Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol 29:204-210, 2000.
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11. Churchill RS, Brems JJ, Kotschi H: Glenoid size, inclination, and version: An anatomic study. J Shoulder Elbow Surg 10:327-332, 2001. 12. Kim SH, Noh KC, Park JS, et al: Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am 87:92-98, 2005. 13. Inui H, Sugamoto K, Miyamoto T, et al: Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res (403):87-92, 2002. 14. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 15. Matsen FA 3rd, Lippitt SB, Sidles JA, Harryman DT 2nd (eds): Practical Evaluation and Management of the Shoulder. Philadelphia, WB Saunders, 1994. 16. Warren RF, Kornblatt IF, et al: Static factors affecting posterior shoulder stability. Orthop Trans 8:89, 1984. 17. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992. 18. Ovesen J, Nielsen S: Anterior and posterior shoulder instability. A cadaver study. Acta Orthop Scand 57:324-327, 1986. 19. Ovesen J, Sojbjerg JO: Posterior shoulder dislocation. Muscle and capsular lesions in cadaver experiments. Acta Orthop Scand 57:535-536, 1986. 20. Weber SC, Caspari RB: A biomechanical evaluation of the restraints to posterior shoulder dislocation. Arthroscopy 5:115-121, 1989. 21. Bey MJ, Hunter SA, Kilambi N, et al: Structural and mechanical properties of the glenohumeral joint posterior capsule. J Shoulder Elbow Surg 14:201-206, 2005. 22. Gerber C, Werner CM, Macy JC, et al: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J Bone Joint Surg Am 85:48-55, 2003. 23. Selecky MT, Tibone JE, Yang BY, et al: Glenohumeral joint translation after arthroscopic thermal capsuloplasty of the posterior capsule. J Shoulder Elbow Surg 12:242-246, 2003. 24. Provencher MT, Bell SJ, Menzel KA, Mologne TS: Arthroscopic treatment of posterior shoulder instability: results in 33 patients. Am J Sports Med 33:1463-1471, 2005. 25. Weinberg J, McFarland EG: Posterior capsular avulsion in a college football player. Am J Sports Med 27:235-237, 1999. 26. Chhabra A, Diduch DR, Anderson M: Arthroscopic repair of a posterior humeral avulsion of the inferior glenohumeral ligament (HAGL) lesion. Arthroscopy 20(Suppl 2):73-76, 2004. 27. Safran O, Defranco MJ, Hatem S, Iannotti JP: Posterior humeral avulsion of the glenohumeral ligament as a cause of posterior shoulder instability. A case report. J Bone Joint Surg Am 86:2732-2736, 2004. 28. Hottya GA, Tirman PF, Bost FW, et al: Tear of the posterior shoulder stabilizers after posterior dislocation: MR imaging and MR arthrographic findings with arthroscopic correlation. Am J Roentgenol 171:763-768, 1998. 29. Kim SH, Ha KI, Yoo JC, Noh KC: Kim’s lesion: An incomplete and concealed avulsion of the posteroinferior labrum in posterior or multidirectional posteroinferior instability of the shoulder. Arthroscopy 20:712-720, 2004. 30. Yu JS, Ashman CJ, Jones G: The POLPSA lesion: MR imaging findings with arthroscopic correlation in patients with posterior instability. Skeletal Radiol 31:396-399, 2002.
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31. Lippitt S, Matsen F: Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res (291):20-28, 1993. 32. Lippitt SB, Vanderhooft JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quantitative analysis. J Shoulder Elbow Surg 2:27-35, 1993. 33. Tibone JE, Bradley JP: The treatment of posterior subluxation in athletes. Clin Orthop Relat Res (291):124-137, 1993. 34. Hovis WD, Dean MT, Mallon WJ, Hawkins RJ: Posterior instability of the shoulder with secondary impingement in elite golfers. Am J Sports Med 30:886-890, 2002. 35. Sauers EL, Borsa PA, Herling DE, Stanley RD: Instrumented measurement of glenohumeral joint laxity and its relationship to passive range of motion and generalized joint laxity. Am J Sports Med 29:143-150, 2001. 36. Silliman JF, Hawkins RJ: Classification and physical diagnosis of instability of the shoulder. Clin Orthop Relat Res (291):7-19, 1993. 37. Tennent TD, Beach WR, Meyers JF: A review of the special tests associated with shoulder examination. Part II: Laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med 31:301-307, 2003. 38. Gerber C, Ganz G: Clinical assessment of instability of the shoulder. With special reference to anterior and posterior drawer tests. J Bone Joint Surg Br 66:551-556, 1984. 39. Kim SH, Park JS, Jeong WK, Shin SK: The Kim test: A novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med 33:1188-1192, 2005. 40. Warren RF, Craig EV, Altchek DW (eds): The Unstable Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1999. 41. Cuéllar R, González J, de la Herrán G, Usabiaga J: Exploration of glenohumeral instability under anesthesia: The shoulder jerk test. Arthroscopy 21:672-679, 2005. 42. Kim SH, Park JC, Park JS, Oh I: Painful jerk test: A predictor of success in nonoperative treatment of posteroinferior instability of the shoulder. Am J Sports Med 32:1849-1855, 2004. 43. Nakagawa S, Yoneda M, Hayashida K, et al: Posterior shoulder pain in throwing athletes with a Bennett lesion: Factors that influence throwing pain. J Shoulder Elbow Surg 15: 72-77, 2006. 44. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409-419, 1987. 45. Borsa PA, Jacobson JA, Scibek JS, Dover GC: Comparison of dynamic sonography to stress radiography for assessing glenohumeral laxity in asymptomatic shoulders. Am J Sports Med 33:734-741, 2005. 46. Beltran J, Rosenberg ZS, Chandnani VP, et al: Glenohumeral instability: Evaluation with MR arthrography. Radiographics 17:657-673, 1997. 47. Tung GA, Hou DD: MR arthrography of the posterior labrocapsular complex: Relationship with glenohumeral joint alignment and clinical posterior instability. Am J Roentgenol 180:369-375, 2003. 48. Magee T, Williams D, Mani N: Shoulder MR arthrography: Which patient group benefits most? Am J Roentgenol 183:969-974, 2004.
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49. Tirman PF, Smith ED, Stoller DW, Fritz RC: Shoulder imaging in athletes. Semin Musculoskelet Radiol 8:29-40, 2004. 50. Volpi D, Olivetti L, Budassi P, Genovese E: Capsulo-labroligamentous lesions of the shoulder: Evaluation with MR arthrography. Radiol Med (Torino) 105:162-170, 2003. 51. Engle RP, Canner GC: Posterior shoulder instability: Approach to rehabilitation. J Orthop Sports Phys Ther 10: 488-494, 1989. 52. Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003. 53. Abrams JS, Savoie FH 3rd, Tauro JC, Bradley JP: Recent advances in the evaluation and treatment of shoulder instability: Anterior, posterior, and multidirectional. Arthroscopy 18(Suppl 2):1-13, 2002. 54. Pearsall AW 4th, Jarrett CA: A salvage procedure for refractory shoulder instability. Clin Orthop Relat Res (431): 245-249, 2005. 55. Metcalf MH, Duckworth DG, Lee SB, et al: Posteroinferior glenoplasty can change glenoid shape and increase the mechanical stability of the shoulder. J Shoulder Elbow Surg 8:205-213, 1999. 56. Chhabra A, Bradley JP, Herzka A, et al: Arthroscopic capsulolabral reconstruction for posterior inferior instability of the shoulder: A prospective study of 100 athletes. Presented at the American Orthopaedic Society for Sports Medicine 2005 Annual Meeting, Keystone, Colo, July 2005. 57. Plancher KD, Johnston JC, Peterson RK, Hawkins RJ: The dimensions of the rotator interval. J Shoulder Elbow Surg 14:620-625, 2005. 58. Fuchs B, Jost B, Gerber C: Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am 82:16-25, 2000. 59. Scarpinato DF, Andrews JR: Posterior instability of the shoulder. In Andrews JR, Wilk KE (eds): The Athlete’s Shoulder. New York, Churchill Livingstone, 1994, pp 205-214. 60. Hawkins RJ, Koppert G, Johnston G: Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am 66:169-174, 1984. 61. Bigliani LU, Pollock RG, McIlveen SJ, et al: Shift of the posteroinferior aspect of the capsule for recurrent posterior glenohumeral instability. J Bone Joint Surg Am 77: 1011-1020, 1995. 62. Bottoni CR, Franks BR, Moore JH, et al: Operative stabilization of posterior shoulder instability. Am J Sports Med 33:996-1002, 2005. 63. Nebelung W, Röpke M, Urbach D, Becker R: A new technique of arthroscopic capsular shift in anterior shoulder instability. Arthroscopy 17:426-429, 2001. 64. Boileau P, Ahrens P: The TOTS (temporary outside traction suture): A new technique to allow easy suture placement and improve capsular shift in arthroscopic bankart repair. Arthroscopy 19:672-677, 2003. 65. Goubier JN, Iserin A, Augereau B: The posterolateral portal: A new approach for shoulder arthroscopy. Arthroscopy 17:1000-1002, 2001. 66. Schneeberger AG, Yian EH: Arthroscopic posterior portal closure. Arthroscopy 20(Suppl 2):110-112, 2004.
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CHAPTER 19 Multidirectional Instability
of the Shoulder John Uribe, John Zvijac, Bashir Zikria, and Angie Botto-van Bemden
Multidirectional instability as a pathologic entity was first described by Carter Rowe in 1956.1,2 He was also the first to focus on the relative atraumatic nature of humeral instability in more than one direction. Today, we recognize multidirectional instability as a major cause of shoulder instability in the athletic population.
static and dynamic restraints help maintain stability while allowing the most motion of any joint in the body. Thorough descriptions of the anatomy and biomechanics of the shoulder in relation to shoulder instability may be found in Chapters 1 and 2. Table 19-1 lists anatomic factors that may affect the stability of the glenohumeral joint.
In 1971, Endo and colleagues3 reported on atraumatic inferior subluxation of the humeral head in relation to the glenoid, which they had observed on radiographs of loaded shoulders. Neer and Foster4 expanded on the concept of degrees of atraumatic multidirectional instability, ranging from mild subluxation to frank dislocation of the humeral head in more than one direction. In 1980, they reported on a series of 36 patients (40 shoulders) with atraumatic instability in multiple directions. All their patients were noted to have involuntary inferior subluxation or dislocation associated with anterior or posterior instability of the shoulder, or both. They defined multidirectional instability as excessive humeral translation in more than one direction. The current literature, however, is inconsistent in its definition of multidirectional instability. As a consequence, the prevalence of this condition remains controversial.
CLINICAL PRESENTATION Patients with multidirectional instability typically present with the shoulder reduced, but complain of pain, a feeling of instability, or both, without a history of significant trauma. The direction of the instability may be determined by the symptoms, even if they are vague. A patient with symptoms produced by carrying heavy objects indicates inferior instability. Symptoms produced while pushing heavy doors—the arm in forward elevation and internal rotation—suggest posterior instability. Traction parasthesias often accompany these symptoms of instability. Patients may also have a history of laxity in other joints, or a ligamentous laxity may be present in other members of the patient’s family. Dowdy and O’Driscoll15 have discovered a 24% probability of instability in family members of patients treated surgically for recurrent anterior shoulder instability. Additionally, collagen disorders such as Ehlers-Danlos syndrome and other biomechanical disorders may manifest with generalized joint laxity.
Accurate use of the term multidirectional is not only essential for proper diagnosis, but also for choosing the appropriate treatment.5 In this chapter, multidirectional instability is defined as symptomatic excessive translation of the humeral head with respect to the glenoid in more than one direction. It is important to distinguish pathologic instability from normal laxity. For example, the sulcus sign is a clinical sign of inferior laxity that may or may not be pathologic; moreover, patients with instability in one direction, who also have generalized ligamentous laxity, should not be classified as having multidirectional instability. Patients who meet the criteria for the definition of multidirectional instability represent diagnostic and therapeutic challenges to the physician and physical therapist.
The physical examination may demonstrate generalized ligamentous laxity in other joints. Multidirectional instability of the opposite shoulder may provide a clue to the origin of instability in the involved shoulder. It is important to assess the acromioclavicular and sternoclavicular joints for tenderness, because they may be a source of hypermobility of the shoulder. Eliciting the glenohumeral translations that reproduce symptoms may be informative. The sulcus sign is an inferior sag of the humerus with the arm in adduction, indicating inferior laxity. Additional tests for laxity include the anterior, inferior, and posterior apprehension signs, relocation tests, and clunk tests. Superior labral anterior-posterior (SLAP) lesions may be clinically diagnosed with the O’Brien or grind test. Table 19-2 lists common tests and their clinical significance for assessing shoulder instability.
ANATOMY AND BIOMECHANICS A thorough comprehension of glenohumeral anatomy and biomechanics is essential to understanding the complex nature of multidirectional instability.6-14 The glenohumeral articulation is an inherently unstable joint. Contributions of
Routine radiographs include an anteroposterior (AP), internal and external rotation views of the humerus, 229
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TABLE 19-1 Anatomic Factors Involved With Glenohumeral Joint Stability Factor
Function
Abnormality
Congruity of articular surface
Concavity-compression effect
Glenoid dysplasia, fracture, Hill-Sachs lesion, reverse Hill-Sachs lesion
Glenoid labrum
Increases depth of socket and surface area; anchoring point for ligaments and capsule
Bankart lesion
Negative intra-articular pressure
Vacuum effect
Capsular rupture, defect of rotator interval, capsular laxity, capsular injury
Coracohumeral ligament–superior glenohumeral ligament
Limits external rotation and inferior translation in adduction, posterior translation in flexion
Lesion of rotator interval
Middle glenohumeral ligament
Limits external rotation and inferior translation in adduction; anterior translation in midabduction
Bankart lesion and capsular injury
Inferior glenohumeral ligament complex
Limits anterior, posterior, and inferior translation in abduction
Bankart lesion and capsular injury
Posterior aspect of the capsule
Limits posterior translation in flexed, adducted, and internally rotated shoulder
Posterior capsular laxity and injury
Rotator cuff
Dynamic joint compression; steering effect
Overuse injury (fatigue) and rupture
Biceps (long head)
Dynamic restraint to anterior and superior Lesion of superior portion of labrum, translation anterior and posterior (SLAP lesion), rupture
Adapted from Warner JJP, Schulte KR, Imhoff AB: Current concepts in shoulder instability. Adv Oper Orthop 3:219, 1995.
scapular Y, and axillary lateral; however, they are often insignificant in a patient with multidirectional instability. They should still be evaluated for any presence of humeral defects, such as a Hill-Sachs lesion, which is best seen on the internal rotation view, or glenoid lesions, seen best on axillary views. Magnetic resonance imaging (MRI) allows visualization of the superficial and deep structures with multiplanar capabilities of the glenohumeral joint. It may be useful in assessing rotator cuff pathology, labral morphology, and osseous integrity. Furthermore, MRI is beneficial if instability results in an injury to the axillary or suprascapular nerves. Denervated muscle demonstrates edema in the acute phase and then atrophy and fatty replacement during the chronic phase. Computed tomography (CT) scans provide a reliable measure of the osseous structures of the shoulder, helping to assess the glenoid version and identify any bony defects that may be difficult to identify on plain radiographs. CT arthrography is an invasive procedure that can be used to define osseous structures as well as labral and capsular integrity. This method, confined predominantly to axial images, has limited planar capabilities when compared with MRI. Ultrasonography offers little visualization of the labrum and capsule. It has been advocated for rotator cuff pathology, but even then it is operator dependent.
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TREATMENT Nonoperative Treatment Multidirectional instability may be treated operatively or nonoperatively. Initially, all patients should attempt conservative management, including activity modification and physical therapy. The goal of nonoperative therapy is to strengthen the scapular stabilizers, rotator cuff, and deltoid muscles. Matsen and Zuckerman16 have studied athletes with loose or lax capsules and found that the stability of the shoulder is dependent on the scapular stabilizers. Additional studies have shown that patients with shoulder instability have imbalances in muscle coordination17 and deficits in proprioception.18 Along with strengthening the muscles, it is important to improve muscle coordination and increase the patient’s functional adaptation. Activity modification entails patients avoiding any movement that might reproduce symptoms of instability. Patients should be informed that subsequent subluxations, or dislocations, of their shoulder increase the probability of recurrence. Strengthening of the rotator cuff, deltoid, and scapula-stabilizing muscles can be accomplished with a series of exercises. Initially, patients are taught to use the shoulder in the most stable position, with the humerus
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TABLE 19-2 Clinical Tests for Instability and Laxity
Diagnostic Test
Provocation
Patient Positioning Arm Positioning
Technique
Outcome
Provocation and Relief Tests for Instability Relocation
Pain and apprehension
Supine
Abducted to 90º and externally rotated to 90º
Humeral head pressed posteriority while arm is externally rotated
Relieves pain and apprehension
Anterior release
Pain and apprehension
Supine
Abducted to 90º and externally rotated to 90º
Same as relocation test, then posterior pressure is suddenly released
Pain and/or apprehension
Apprehension
Pain and apprehension
Sitting or standing
90º abduction and full external rotation
Arm is externally rotated while pressure is applied anteriorly to humeral head
Pain and/or apprehension
Clunk
Clunk or grinding
Supine
Full abduction
Arm is rotated in full external rotation, caput human is pushed slightly in anterior direction
Clunk or grinding
Laxity Tests for Instability Load and shift anterior or posterior
Anterior or posterior laxity
Sitting, standing, or supine
Neutral position
Humeral head is fixed by clinician’s hand, clinician tries to shift humeral head in anterior (or posterior) direction
Does not evoke discomfort: degree of humeral head translation on the glenoid in different positions of the humerus is evaluated using the Hawkins grading scheme*
Sulcus sign
Inferior laxity
Sitting or standing
Neutral position
Arm is pulled vertically downward
Positive when sulcus becomes visible between acromion and humeral head
Provocation and Relief Tests for Labral Tears Biceps load I
Pain
Supine
Arm is 90º abducted, elbow is 90º flexed
Clinician applies flexion pressure as patient resists
Positive if pain occurs
Biceps load II
Pain
Supine
120º abduction
Clinician applies lateral force as patient resists
Positive if pain occurs
Mimori
Pain and apprehension
Sitting or standing
Arm is 90º abduction, elbow is 90º flexed, forearm is supined
Forearm is brought from maximum supination to maximum pronation
Positive if pain occurs
Zaslav
Compares strength Sitting or standing in internal rotation with that of external rotation, excluding impingement from labral tears
Arm is in 90º abduction and 80º external rotation, elbow is 90º flexed
Patient resists external rotation force applied by the clinician, followed by applied internal rotation force
Positive (labral tear present) when the patient has good strength against external rotation and apparent weakness against internal rotation
Continued
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TABLE 19-2 Clinical Tests for Instability and Laxity—cont’d
Diagnostic Test
Provocation
Patient Positioning Arm Positioning
Technique
Outcome Positive if pain elicited with first maneuver, is reduced or eliminated in the second
Active compression Pain and relief (O’Brien)
Sitting or standing
Arm is in 90º forward flexion and 10º-15º abduction and full internal rotation
Clinician stands in front of patient. Arm is pushed down as patient resists. Repeated with arm in external rotation
Compression rotation
Pain or clicking
Supine
Arm at 90º abduction, elbow in 90º flexion
Positive if pain or Axial load placed on clicking occurs shoulder while rotated and circumducted (note McMurray knee test)
SLAP-prehension
Pain or clicking
Sitting or standing
Arm at 90º forward flexion
Arm is rotated internally in 90º flexion of the humerus
Positive if pain or clicking occurs
Speed
Pain in the anterior shoulder
Sitting or standing
90º elevation
Downward force applied to forearm, full supination of forearm and elbow is fully extended
Positive if pain occurs
Tenderness of bicipital groove
Pain
Sitting
Neutral
Palpating the bicipital groove
Positive if pain occurs
Yergason
Pain in the biceps tendon
Sitting with elbow at 90º
Neutral
Patient supinates forearm against clinician’s resistance, who simultaneously palpates biceps tendon
Positive if pain occurs
SLAP, superior labral anterior-posterior. * Hawkins grading scheme: grade 0 denotes little to no movement: grade 1 denotes the humeral head moves onto the glenoid rim; grade 2 indicates the humeral head can be dislocated-but spontaneously relocates: and grade 3 indicates the humeral head does not relocate when the pressure is removed in the Hawkins scheme, grades 1 to 3 are seen as positive outcomes on a laxity test. From Luime JJ, Verhagen AP, Miedema HS, et al: Does this patient have an instability of the shoulder or a labrum lesion? JAMA 292:1989-1999, 2004.
positioned in the plane of the scapula. It is thought that performing strengthening exercises in the scapular plane enhances muscle force by optimizing the length-tension relationship of the deltoid and rotator cuff musculature. Furthermore, in this position, less stress is placed on the anterior and posterior capsule. As muscle strength and coordination improve, the shoulder is brought into less intrinsically stable positions. Strengthening exercises for the rotator cuff muscles are performed by maintaining the humerus in close proximity to the body while rotating it against resistance. Push-ups and shoulder shrugs also assist in strengthening the scapular stabilizers. Jobe and associates19 have further emphasized the benefits of including isometric exercises as part of the rehabilitation program. If isotonic exercises are performed, they should initially be performed in a limited range of motion to avoid irritating the joint capsule and ligaments. Neuromuscular patterns required for stability are learned again through smooth repetitive motions such as swimming. To prevent further irritation during
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rehabilitation, a brief course of nonsteroidal antiinflammatory drugs (NSAIDs) may be used. NSAIDs may also help if the instability causes a secondary bursitis or rotator cuff tendonitis. The outcomes of rehabilitation are much more promising in atraumatic instability as compared with traumatic instability. Burkhead and Rockwood20 have compared traumatic versus atraumatic instability in 140 shoulders. Only 12 of 74 shoulders (16%) with a traumatic instability had a good or excellent postexercise outcome. In patients with atraumatic instability, 53 of 66 shoulders (80%) had a good or excellent outcome with rehabilitation. They also reported that rehabilitation may even be successful in multidirectional instability secondary to congenital factors. Ide and coworkers21 have reported on shoulder-strengthening exercises with an orthosis on 73 shoulders with multidirectional instability at a mean follow-up of 7 years. Most patients demonstrated significant improvements in strength, with only 3 patients not responding to conservative management and requiring surgery.
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Not all studies reported positive patient outcomes following conservative management. Misamore and colleagues22 have recently reported poor results following conservative treatment in young athletic patients diagnosed with multidirectional instability. Poor outcomes were seen in 19 of 36 patients, with only 8 patients demonstrating freedom from pain and instability with nonsurgical management.
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Flatow23 have recommended the anterior approach for shoulders that dislocate anteriorly and posteriorly.
Open Surgical Procedures The gold standard procedure in the literature is the inferior capsular shift, as described by Neer and Foster in 1980.4 The inferior capsular shift reduces the capsular volume of the glenohumeral joint inferiorly, anteriorly, and posteriorly by equilibrating capsular tension on all sides and balancing the humeral head (Fig. 19-1). The approach for the capsular shift may be anterior or posterior; this may be determined by the patient’s history and a physical examination. The side with the greatest clinical instability should be addressed using the surgical approach. Yamaguchi and
Anterior Approach. The skin incision for the anterior approach is an axillary incision from the tip of the coracoid to the inferior border of the pectoralis major. The deltopectoral interval is identified and the cephalic vein taken laterally, because there are fewer branches laterally than medially.24 The pectoralis major is retracted medially and the deltoid is retracted laterally. The clavipectoral fascia is incised lateral to the strap muscles. The subscapularis muscle is identified with the arm in a slight degree of external rotation to assist in identifying the superior and inferior borders of the muscle. The subdeltoid bursa is excised and the insertion of the subscapularis tendon is identified on the lesser tuberosity. The anterior humeral circumflex vessels are cauterized on the inferior border of the subscapularis. The subscapularis tendon is taken down 1 cm medial to its insertion on the lesser tuberosity from the rotator interval to the lower border of the tendon. The subscapularis tendon is lifted off the capsule and retracted medially, with stay sutures placed in the tendon. Occasionally, one half of the tendon remains attached to the capsule in an effort to reinforce the anterior aspect of the capsule when the tissue is thin or weak. A T-shaped incision is made in the capsule. The vertical segment of the T is just medial to the capsular attachment on the humerus. The superior flap contains the superior and middle glenohumeral ligaments, whereas the inferior glenohumeral ligament is contained within the inferior flap. The inferior flap is then shifted superiorly to eliminate the inferior redundancy and tension on the posterior capsule. The superior flap is pulled downward and sutured to the soft tissue of the humerus. The capsule is repaired with the arm in external rotation and abduction. The amount of external rotation and abduction is modified and determined according to the patient. For example, the dominant arm in throwing athletes would require more abduction and external rotation. Altchek and associates25 have described a similar approach to the T-plasty, basing the capsular incision on the glenoid rim (Fig. 19-2). According to their study, this technique allows for simultaneous Bankart repair and capsular shift.
Figure 19-1. Inferior capsular shift. (From Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980.)
Posterior Approach. In the posterior approach, a vertical incision is made midway between the lateral border of the acromion and the posterior axillary crease. The deltoid is split to expose the tendons of the infraspinatus and teres minor, developing an interval within the infraspinatus muscle without dividing its tendon. Caution is used to avoid dissecting below the infraspinatus, allowing the axillary nerve and posterior humeral circumflex vessels to remain intact. The posterior capsule is identified and a T-shaped capsular incision is made medially, near the glenoid (Fig. 19-3). The inferior limb is advanced medially and superiorly to eliminate the posterior inferior capsular redundancy. The capsule is reattached to the glenoid using suture anchors.
Generally, the standard of care involves a 6- to 12-month period of rehabilitation as initial treatment for multidirectional instability. If the patient fails conservative management—pain and instability persist—operative intervention may then be considered.
Operative Treatment The decision to operate on a patient with multidirectional instability should only be considered if pain and instability persist following an adequate rehabilitation program (minimum of 6 months’ duration). The patient’s symptoms, cause, and level of activity must also be carefully considered. Operative interventions for multidirectional instability include open and arthroscopic procedures. Because the primary pathology in multidirectional instability is the loose redundancy of the capsule, standard surgical procedures for unidirectional instability are inadequate because they fail to address this excessive redundancy. Operative intervention for multidirectional instability attempts to reduce the total capsular volume.
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The results of the inferior capsular shift have been promising for multidirectional instability. Neer and Foster4 have reported a successful outcome, with a failure of only 1 in 32 patients (3%). They later reported similar results on 100 additional capsular shifts. Altchek and associates25 have reported 90% patient satisfaction on 42 shoulders with the T-plasty procedure. Pollock and coworkers26 have reported successful outcomes on 52 shoulders with an inferior capsular shift, with a mean follow-up of 61 months. Their results demonstrated the efficacy and durability of the inferior capsular shift for multidirectional instability. Figure 19-2. T-plasty modification of Bankart procedure. (From Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone and Joint Surg Am 73:105-112, 1991.)
Most surgeons prescribe immobilization in a sling for approximately 6 weeks postoperatively. Passive and active range-of-motion exercises begin between 6 to 12 weeks. At 3 months, the patient may begin strengthening exercises and, at 6 months, throwing. Patient participation in sports is only permitted once full range of motion and strength have returned.
B
A
Figure 19-3. Posterior inferior capsular shift. The teres minor musculotendinous unit is not detached. Dissection is performed between the infraspinatus tendon and capsule. The capsule is opened with a T-shaped incision, creating a superior flap (A) and an inferior flap (B). The superior flap is then shifted inferiorly and the inferior flap is shifted superiorly. (From Fuchs B, Jost B, Gerber C: Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am 82:16-25, 2000.)
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The complication most often reported for inferior capsular shift for multidirectional instability is recurrent instability. Additional complications have included axillary nerve neuropraxia, brachial plexus injuries, and capsular contractures. Arthroscopic Surgical Procedures In recent years, arthroscopic suture capsulorrhaphy and thermal capsulorrhaphy have yielded a high percentage of patient satisfaction for multidirectional instability. Detrisac and Johnson27 pioneered the use of arthroscopic techniques for treating shoulder instability. In 1997, McIntyre, and colleagues28 described modified arthroscopic techniques to accomplish the same stabilizing vertical shift of the capsule as Neer had demonstrated with his open capsular shift. Hewitt and associates29 have continued modifying arthroscopic techniques, describing the use of anchors and sutures and developing an all-inside technique for the treatment of multidirectional instability. The indications for arthroscopic stabilization of multidirectional instability are similar to those for the open procedure. The arthroscopic technique should address the capsular laxity and also correct secondary changes from the continuing symptomatic subluxation and dislocation of the shoulder. For example, associated capsulolabral tears or avulsions should be repaired concomitantly. The potential to identify and treat concomitant pathologies is one of the major advantages of arthroscopic versus open repair. Additional advantages include lower morbidity, reduced pain, shorter surgical time, and improved cosmesis. The patient is placed in the lateral or beach chair position for the arthroscopic procedure. The standard posterior portal is made and the arthroscope introduced into the joint. Two anterior portals are made using an outside-in technique. It is imperative to have these utility portals in the proper position because they function for instrument passage, glenoid preparation, suture management, and knot tying. The anterior superior portal is made just underneath the biceps tendon and the anterior inferior portal is made just above the subscapularis tendon (Fig. 19-4). A diagnostic arthroscopy is performed from the posterior and anterior portals. Suture anchors are placed on the glenoid rim from inferior to superior. The first anchor is critical in establishing proper capsular tension. After mobilization of the capsulolabral periosteal sleeve, it is usually
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235
often have significant inferior laxity when the arm is in adduction and external rotation during the physical examination. This interval lies within the anterior and superior capsular region, between the anterior border of the supraspinatus tendon and superior border of the subscapularis tendon. The superior and middle glenohumeral ligaments are the major ligamentous components of the rotator interval. If the shoulder still demonstrates persistent inferior or inferoposterior translation after the arthroscopic capsular shift, the rotator interval should be closed. Wolf and colleagues.31 have demonstrated on cadaveric shoulders that closure of the rotator interval significantly decreases laxity in all planes of the glenohumeral joint. Specifically, closure of the rotator interval decreases anterior, posterior, and inferior translation by 17%, 15%, and 28%, respectively, when compared with untreated shoulders in their study.
Figure 19-4. Schematic of portal placement for arthroscopic stabilization. This illustration of portal placement shows the relation of the two anterior portals relative to the subscapularis and biceps tendons. (From Cohen B, Cole B, Romeo A: Thermal capsulorrhaphy of the shoulder. Oper Tech Orthop 11:38-45, 2001.)
placed in the 5-o’clock position. Appropriate suture management is imperative to prevent loosening of the suture from the anchor. There are many techniques and devices for passing sutures through the tissue. The device of the surgeon’s preference should be placed through the capsulolabral complex medial and inferior to the lowest anchor in order for the entire inferior glenohumeral ligament to shift superiorly and laterally onto the glenoid rim. A minimum of two or three anchors is often needed for an arthroscopic shift beginning from inferior to superior. Recently, Alberta and coworkers30 have reported on arthroscopic anterior-inferior suture plications in the cadaveric model. They described a glenoid-based anterior-inferior capsular plication in a direct medial to lateral direction, with no attempt to advance the capsule superiorly. The surgical technique consists of placing suture anchors just medial to the labrum at the 5-o’clock position and at the superior border of the anterior-inferior glenohumeral ligament. Arthroscopic knots are tied, beginning with the inferior anchor, to complete the capsulorrhaphy. The capsular plication effectively reduces anterior and posterior glenohumeral translation. Anterior translation is consistently reduced by more than 60%. The loss of external rotation is similar to that of open capsular shifts and is among the lowest reported in the literature. Insufficiency within the region of the capsule known as the rotator interval has received attention recently because of some failed arthroscopic techniques attributed to this disorder. Patients with rotator interval lesions
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The outcomes of arthroscopic surgery should be compared with the gold standard, inferior capsular shift. McIntyre and associates28 have reported on 19 patients with multidirectional instability; 14 of the 19 patients were athletes. One patient had recurrent instability; 13 of the 14 athletes returned to their previous level of performance. Treacy and coworkers32 have reported an average follow-up of 60 months for 25 patients who underwent arthroscopic capsular shifts. Of these patients, 88% were satisfied with the procedure, with only 3 of 25 (12%) reporting continued instability. Their results were similar to those reported for inferior capsular shift. The major complications reported with arthroscopic capsular shifts have been with recurrent instability. There is less risk of injuring the axillary nerve and reducing motion, by preserving the subscapularis tendon on the lesser tuberosity. Thermal Capsulorrhaphy. If capsular laxity persists after the capsulolabral repair translation, persistent laxity may be reduced using thermal capsulorrhaphy. Heat treatment for multidirectional instability was introduced during the past decade. Initial interest, however, has steadily declined because of inconsistent results. Thermal energy works on the type I collagen of ligaments and joint capsules. The heating of collagen breaks the intramolecular cross-links, denaturing the protein. The collagen undergoes a transition from a highly organized state to a random gelatinous state because of the cumulative effect of the unwinding riple helices and residual tension of the heat-resistant intermolecular bonds working in concert to shrink collagen. The initial degree of shrinkage is directly related to the rate and amount of heat applied. Studies have demonstrated that this shrinkage reduces the joint capsule volume. Early on, Hayashi and colleagues33 showed the potential benefits of heat treatment for shoulder instability. They reported a significant decrease in capsular laxity after heat treatments in rabbits. Karas and associates34 have reported reduced capsular volume by 34% alone and 41% when used in combination with capsular plication in the cadaver
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model. Conversely, Luke and coworkers35 have compared the difference in reduction of capsular joint volume of an open capsular shift with thermal capsulorrhaphy in the cadaveric model; the open capsular shift reduces capsular volume by 50% compared with a 30% reduction for thermal capsulorrhaphy. As noted, the capsular response is dependent on temperature and rate. The technique for thermal capsulorrhaphy begins with the speed at which the probe is moved across the tissue and the areas of application (Fig. 19-5). Areas with the highest amount of collagen density will respond the most, such as the inferior glenohumeral ligaments. It is of utmost importance not to leave the probe in one position to prevent significant injury to the capsule. Fanton36 has shown encouraging results for shoulder instability with thermal capsular shrinkage; the study of 54 patients had a success rate higher than 90%, with a minimum follow-up of 2 years. Levitz and colleagues34 have reported successful results of using thermal capsulorrhaphy in overhead athletes; 90% returned to their preinjury
level of competition. Two other studies by Fitzgerald38 and Noonan39 and their associates have reported approximately 80% success rates with thermal capsulorrhaphy, although both these studies had short-term follow- up. Conversely, the results of Levy and colleagues40 were not as promising. They reported a significant failure rate for thermal capsulorrhaphy in patients with multidirectional instability—a 36.1% failure rate with laser-assisted capsulorrhaphy over a 40-month follow-up. D’Alessandro and associates41 have reported on 84 shoulders with instability and found a high rate of unsatisfactory overall results (37%), with an average follow of 38 months. Finally, Miniaci and McBirnie42 have studied 19 patients with multidirectional instability and found that thermal capsular shrinkage has a substantial failure rate, with associated postoperative complications. Complications included recurrence of instability (9 patients), stiffness (5 patients), and neurologic symptoms (4 patients). Complications from thermal capsulorrhaphy include shoulder stiffness, cartilage damage, capsular necrosis, axillary nerve injury, and failure of the procedure itself. Park and coworkers43 have shown that in 14 patients with failed thermal capsulorrhaphy, capsular thinning or necrosis often occurs (43%). They were able to perform revision surgery with the remaining capsular tissue using an open subscapularis splitting technique. It was concluded that recurrent laxity after thermal capsulorrhaphy is common, but in most cases the capsule quality does not affect the revision procedure. Postoperative rehabilitation after arthroscopic repair is identical to that after open reconstruction. Sling immobilization generally is required for 4 to 6 weeks, depending on the methods used and the instability pattern treated. In roughly 6 to 12 weeks, patients begin passive and active range-of-motion exercises. The patient is generally allowed to return to sports participation in 18 to 36 weeks.
SUMMARY
Figure 19-5. Arthroscopic thermal capsulorrhaphy after anterior stabilization with suture anchors. A monopolar radiofrequency device (OraTec Interventions, Menlo Park, Calif) may be used to reduce capsular volume additionally after an arthroscopic Bankart repair. A grid technique is used to treat the capsule. Care is taken to avoid thermal treatment near the suture line to avoid weakening the surgical repair. Treatment of the capsule (gray shaded area) within the regions of the middle, inferior, and posterior glenohumeral ligaments may be required, depending on the degree of capsular laxity. Thermal treatment of the axillary pouch is avoided entirely. (From Cohen B, Cole B, Romeo A: Thermal capsulorrhaphy of the shoulder. Oper Tech Orthop 11:38-45, 2001.)
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Multidirectional instability is more prevalent than previously thought. It is imperative to have an accurate definition for multidirectional instability prior to diagnosis and appropriate treatment. The diagnosis may be derived on the basis of a careful history and physical examination. Radiographs, such as an MRI or CT scan, are helpful in identifying associated pathology with multidirectional instability. Most patients may be treated conservatively with an appropriate rehabilitation program of 6 months’ minimum duration. Surgery is only indicated for those patients who fail to respond to conservative treatment. The gold standard surgical procedure is Neer’s open inferior capsular shift. All other surgical procedures, such as arthroscopic capsular shifts, should be compared with the gold standard. In recent years, with the advance of arthroscopic techniques, the results of both procedures are similar.
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References 1. Rowe CR: Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 38:957-977, 1956. 2. Rowe CR: Acute and recurrent dislocations of the shoulder. J Bone Joint Surg Am 44:998-1008, 1962. 3. Endo H, Takigawa H, Takata K, Miyoshi S: A method of diagnosis and treatment of the loose shoulder. Cent Jpn J Orthop Trav Surg 14:630, 1971. 4. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980. 5. McFarland EG, Kim TK, Park HB, et al: The effect of variation in definition on the diagnosis of multidirectional instability of the shoulder. J Bone Joint Surg Am 85:2138-2144, 2003. 6. Kondo T, Hashimoto J, Nobuhara K, Takakura Y: Radiographic analysis of the acromion in the loose shoulder. J Shoulder Elbow Surg 13:404-409, 2004. 7. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop 285: 181-190, 1992. 8. Howell, SM, Galinat, BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop 243:122-125, 1989. 9. Inui H, Sugamoto K, Miyamoto T, et al: Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res (403):87-92, 2002. 10. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 11. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 12. Terry GC, Hammon D, France P, Norwood LA: The stabilizing function of passive shoulder restraints. Am J Sports Med 19:26-34, 1991. 13. Pollock RG, Bucchieri JS, Wang VM, et al: Subfailure repetitive loading of the IGHL affects its mechanical properties. Trans Orthop Res Soc 22:164, 1997. 14. Boardman ND, Debski RE, Warner JJ, et al: Tensile properties of the superior glenohumeral and coracohumeral ligaments. J Shoulder Elbow Surg 5:249-254, 1996. 15. Dowdy PA, O’Driscoll SW: Shoulder instability. An analysis of family history. J Bone Joint Surg Br 75:782-784, 1993. 16. Matsen FA III, Zuckerman JD: Anterior glenohumeral instability. Clin Sports Med 2:319-338, 1983. 17. Kronberg M, Broström LÅ, Németh G: Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop, 269:181-192, 1991. 18. Lephart SM, Warner JJP, Borsa PA, et al: Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulders. J Shoulder Elbow Surg 3:371-380, 1994. 19. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 20. Burkhead WZ Jr, Rockwood CA Jr: Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am 74:890-896, 1992. 21. Ide J, Maeda S, Yamaga M, et al: Shoulder-strengthening exercise with an orthosis for multidirectional shoulder instability: Quantitative evaluation of rotational shoulder strength before and after the exercise program. J Shoulder Elbow Surg 12:342-345, 2003.
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22. Misamore GW, Sallay PI, Didelot W: A longitudinal study of patients with multidirectional instability of the shoulder with seven- to ten-year follow-up. J Shoulder Elbow Surg 14:466-470, 2005. 23. Yamaguchi K, Flatow EL: Management of multidirectional instability. Clin Sports Med 14:885-902, 1995. 24. Radkowski CA, Richards RS, Pietrobon R, Moorman CT III: An anatomic study of the cephalic vein in the deltopectoral shoulder approach. Clin Orthop Relat Res 442:139-142, 2006. 25. Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone and Joint Surg Am 73:105-112, 1991. 26. Pollock RG, Owens JM, Flatow EL, Bigliani LU: Operative results of the inferior capsular shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am 82:919-928, 2000. 27. Detrisac DA, Johnson LL; Arthroscopic shoulder capsulorrhaphy using metal staples. Orthop Clin North Am 24: 71-88, 1993. 28. McIntyre LF, Caspari RB, Savoie FH III: The arthroscopic treatment of multidirectional shoulder instability: Two-year results of a multiple suture technique. Arthroscopy 13: 418-425, 1997. 29. Hewitt M, Getelman MH, Snyder SJ: Arthroscopic management of multidirectional instability: Pancapsular plication. Orthop Clin North Am 34:549-557, 2003. 30. Alberta FG, Elattrache NS, Mihata T, et al: Arthroscopic anteroinferior suture plication resulting in decreased glenohumeral translation and external rotation. Study of a cadaver model. J Bone Joint Surg Am 88:179-187, 2006. 31. Wolf RS, Zheng N, Iero J, Weichel D: The effects of thermal capsulorrhaphy and rotator interval closure on multidirectional laxity in the glenohumeral joint: A cadaveric biomechanical study. Arthroscopy 20:1044-1049, 2004. 32. Treacy SH, Savoie FH III, Field LD: Arthroscopic treatment of multidirectional instability. J Shoulder Elbow Surg 8: 345-350, 1999. 33. Hayashi K, Thabit G III, Vailas AC, et al: The effect of nonablative laser energy on joint capsular properties. An in vitro histologic and biochemical study using a rabbit model. Am J Sports Med 24:640-646, 1996. 34. Karas SG, Creighton RA, DeMorat GJ: Glenohumeral volume reduction in arthroscopic shoulder reconstruction: a cadaveric analysis of suture plication and thermal capsulorrhaphy. Arthroscopy 20:179-184, 2004. 35. Luke TA, Rovner AD, Karas SG, et al: Volumetric change in the shoulder capsule after open inferior capsular shift versus arthroscopic thermal capsular shrinkage: A cadaveric model. J Shoulder Elbow Surg 13:146-149, 2004. 36. Fanton GS: Arthroscopic electrothermal surgery of the shoulder. Oper Tech Sports Med 6:139-146, 1998. 37. Levitz CL, Dugas J, Andrews JR: The use of arthroscopic thermal capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy 17:573-577, 2001. 38. Fitzgerald BT, Watson BT, Lapoint JM: The use of thermal capsulorrhaphy in the treatment of multidirectional instability. J Shoulder Elbow Surg 11:108-113, 2002. 39. Noonan TJ, Tokish JM, Briggs KK, Hawkins RJ: Laserassisted thermal capsulorrhaphy. Arthroscopy 19:815-819, 2003.
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40. Levy O, Wilson M, Williams H, et al: Thermal capsular shrinkage for shoulder instability. Mid-term longitudinal outcome study. J Bone Joint Surg Br 83:640-645, 2001. 41. D’Alessandro DF, Bradley JP, Fleischli JE, Connor PM: Prospective evaluation of thermal capsulorrhaphy for shoulder instability: Indications and results, two- to five-year follow-up. Am J Sports Med 32:21-33, 2004.
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42. Miniaci A, McBirnie J: Thermal capsular shrinkage for treatment of multidirectional instability of the shoulder. J Bone Joint Surg Am 85:2283-2287, 2003. 43. Park HB, Yokota A, Gill HS, et al: Revision surgery for failed thermal capsulorrhaphy. Am J Sports Med 33:1321-1326, 2005.
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CHAPTER 20 Management of the First-Time
Shoulder Dislocation in the Athlete Robert Y. Wang, Augustus D. Mazzocca, James Bicos, and Robert A. Arciero
Acute traumatic anterior shoulder dislocation is a relatively common occurrence, especially in the athletic population. There are various options available when advising patients about treatment. This chapter will discuss the classification, pathoanatomy, causes, epidemiology, diagnosis, and treatment considerations for the first-time anterior shoulder dislocation.
glenoid hypoplasia and disorders of collagen structure that result in excessive joint laxity. The active mechanisms involved with glenohumeral stability are primarily provided by the rotator cuff muscles. The type and severity of pathoanatomic lesions may be influenced by the patient’s age, mechanism of injury, and degree of trauma.
Bankart Lesion
CLASSIFICATION
The inferior glenohumeral ligament (IGHL) complex is the primary ligamentous restraint to anterior glenohumeral translation, specifically with the arm in an abducted and externally rotated position (Fig. 20-1).3 The specific anatomy of the IGHL has been described as having anterior and posterior bands, with an intervening axillary pouch. Detachment of the anterior-inferior labrum and capsule, comprising the anterior band of the IGHL as a capsulolabral complex, is considered one of the major pathoanatomic features of traumatic anterior shoulder instability.4 Up to 85% of traumatic anterior shoulder dislocations can be associated with detachment of the anterior-inferior labrum and capsule. Broca and Hartman first described the lesion in 1890, followed by Perthes in 1906 and Bankart in 1923. This lesion has subsequently been named the Perthes-Bankart lesion (Fig. 20-2).
Although we will focus on acute traumatic anterior dislocation, it is important to recognize the spectrum of presentation in shoulder instability. Traumatic anterior dislocation would therefore represent one extreme end of the spectrum, as described by Matsen.1 The patient with hyperlaxity, bidirectional instability, and little or no provocation for symptoms would represent the other end. The surgeon should recognize the great degree of crossover that can be observed between these two ends of the spectrum. For example, a hyperlax patient can present with a traumatic dislocation. Understanding the variability of presentation and the unique anatomic and individual characteristics in each patient will lead to optimum treatment. By definition, an acute anterior dislocation is one that requires a reduction; a traumatic instability event can also occur as a subluxation. Spontaneous reduction in this case is oftentimes reported by the athlete as a sensation of a definite clunk and relief of pain. Rowe described this phenomenon as the “dead arm” syndrome, as transient anterior subluxation results in a sudden sharp or “paralyzing” pain where the arm becomes weak or “goes dead.”20 Other classification systems include the direction of instability and timing (acute, recurrent, or chronic).
The mechanism of how the Bankart lesion leads to instability has been studied extensively. The detachment of the labrum from the anterior-inferior glenoid is the essential lesion leading to anterior instability. By displacing the anterior labrum, glenoid depth is decreased by up to 50% and passive restraints, such as the concavity-compression mechanism discussed earlier, are also lost.5,6 Lazarus6 has demonstrated that detachment of the anterior inferior labrum and capsule from the glenoid results in nearly doubling of glenohumeral anterior translation. A Bankart repair is then performed, repairing the anterior IGHL and labrum back to the glenoid, and restoring glenohumeral stability. In another cadaver study, Bigliani has demonstrated that the strain before failure for all boneligament-bone preparations of the shoulder capsule was 27%; the authors concluded that plastic deformation of the capsule is a fundamental component of anterior instability. This is an important concept for the treatment of anterior instability because, in addition to repair of the glenoid labrum, capsular redundancy may require plication, especially in the recurrent instability situation.
PATHOANATOMY The overall stability of the glenohumeral joint involves passive and active mechanisms. Passive or static factors include joint conformity, adhesion and cohesion, finite joint volume, and ligamentous restraints, including the labrum.1 The ligaments and capsule are aided by receptors that provide proprioceptive feedback. When capsuloligamentous structures are damaged, alterations in proprioception occur that are partially restored with operative repair.2 Static stabilizers are also affected by congenital factors; these include 239
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AILC
IGHL
Figure 20-1. Cadaveric images. Shown are the inferior glenoid humeral ligament (IGHL) and anterior inferior labral complex (AILC).
The incidence of a Bankart lesion in the athlete who sustains an anterior dislocation has been studied extensively. Its incidence in the initial dislocation has been reported to be 87% to 100%.8-11 Neviaser, in 1993, added a differentiation between the Bankart lesion and what he termed the anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion (Fig. 20-3).12 In this description of acute and chronic anterior dislocations, the capsule and labrum are not detached as in a Bankart lesion, but the anterior IGHL, labrum, and anterior scapular periosteum are stripped and displaced in a sleevetype fashion medially on the glenoid neck. This is an important diagnostic variant to recognize because in a chronic situation, a cursory inspection of the anterior inferior quadrant of the glenoid may not reveal evidence of trauma. However, closer inspection more medially will show a large, medially displaced labrum on the anterior portion of the glenoid neck.
Capsulolabral complex
Superior Labrum Extension An arthroscopic shoulder examination frequently leads to observations of additional lesions associated with anterior instability. Arciero and coworkers13 have described injuries that may also extend superiorly into the attachment of the biceps tendon, producing a concomitant superior labrum anterior-posterior (SLAP) lesion (Fig. 20-4). This lesion is generally observed when the dislocation involves an extreme type of trauma. In a variation of the anterior superior labrum lesion, the anterior supraspinatus can have partial or complete tears, resulting in varying amounts of instability. This has been called the SLAC lesion (superior labrum, anterior cuff)14; it can be observed in acute and chronic trauma.
Glenoid
Figure 20-2. Bankart lesion. This is an arthroscopic view of the left shoulder, viewed posteriorly, with the patient in a sitting position.
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Figure 20-3. Arthroscopic view of an anterior labrum periosteal sleeve avulsion (ALPSA) lesion. This is an anterior view of the left shoulder, with the lesion being mobilized.
Figure 20-4. Arthroscopic view of a superior labral anterior-posterior (SLAP) lesion, type IV.
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MANAGEMENT OF THE FIRST-TIME SHOULDER DISLOCATION IN THE ATHLETE
Humeral Avulsion of Glenohumeral Ligament Lesions A third type of lesion that can be observed is a lateral detachment of the IGHL from the humeral neck. This has been described by Nicola15 as a humeral avulsion of the glenohumeral ligament (HAGHL) lesion (Fig. 20-5); its proposed mechanism was also discussed. Richards and Burkhart16 have described an all-arthroscopic technique using suture anchors to repair HAGHL lesions, and noted that it is a difficult and demanding technique. Wolf17 has found an incidence of 9.3% in a series of patients presenting with recurrent anterior instability and also described an arthroscopic technique for repair of HAGHL lesions. In this procedure, a standard anterior inferior portal is made, and the bone at the anterior inferior aspect of the humeral neck is burred through this portal. An anterior lateral portal is created 2 cm lateral
A
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and 2 cm inferior to the coracoid process. A suture hook is used to place monofilament absorbable sutures through the capsule; these are tied through the anterior lateral portal over the subscapularis tendon. Bokor and associates18 have reported on 41 cases of HAGHL lesions in 547 shoulders, with an overall incidence of 7.5%. In 2002, Bui-Mansfield19 published a retrospective review of 307 patients with anterior instability; they identified six HAGHL lesions, an incidence of 2%. Although relatively rare, this lesion must be sought for during any anterior instability arthroscopic examination. Taylor and Arciero have also described HAGHL lesions after acute anterior dislocations.10
Traumatic Bone Lesions Traumatic glenoid and humeral head fractures can occur with an anterior shoulder dislocation. The anatomy of the glenoid and proximal humerus is consistent. The articular surface of the proximal humerus is similar to that of a sphere. It is composed of cartilage and subchondral and trabecular bone that is relatively soft, even in young athletes. The glenoid has a consistent morphology as well. It is pear-shaped, with the inferior portion approximating that of a true circle. Bone loss should not be overlooked in any anterior instability event. Even with transient anterior subluxation, Rowe found 15 of 32 breakout lesions involved avulsion of the anterior glenoid rim.20 Studies have shown the average superior-inferior glenoid diameter to be 30.4 to 42.6 mm in males and 29.4 to 37.0 mm in females. Bony lesions of the glenoid or humeral head place greater demand on the integrity of soft tissue repairs and have been shown to cause recurrent anterior instability of the shoulder.21
Humeral Head Lesions
B Figure 20-5. Humeral avulsion of the glenohumeral ligament (HAGHL) lesion. A, Arthroscopic view of HAGHL, sitting position, posterior left shoulder. The subscapularis muscle is seen as a shadowed area in the background. B, Open example of HAGHL lesion, right shoulder. The subscapularis is tagged with suture to the right. The HAGHL lesion is tagged with sutures inferiorly.
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The Hill-Sachs lesion is found on the humerus. This is an impression fracture caused by the humeral head being dislocated anteriorly and impacting on the anterior glenoid. It is generally located at the posterior-superior portion of the humeral head. Burkhart and De Beer21 have reported and defined what they describe as an engaging Hill-Sachs lesion, which catches and locks the humeral head in a functional position of abduction and external rotation. The long axis of the Hill-Sachs lesion is parallel to the glenoid and engages its anterior corner. The nonengaging Hill-Sachs lesion passes diagonally across the anterior glenoid with external rotation so that there is continual contact between the articular surfaces. These shoulders are reasonable candidates for arthroscopic Bankart repair. It is important to realize, however, that the Hill-Sachs lesion is created by the position of the arm when the dislocation occurs. A Hill-Sachs lesion that develops with the arm at the side with some extension of the shoulder will be located more vertically and superiorly
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than the lesion that occurs with the shoulder abducted and externally rotated. The Hill-Sachs lesion that develops with the arm at the side is generally a nonengaging lesion. Norlin9 has shown that in Hill-Sachs lesions, 25% of cases are down to subchondral bone and 75% are just chondral lesions. Taylor and Arciero10 have show that of 57 patients with Hill-Sachs lesions, 23 were chondral and 34 were osteochondral. None of these lesions was large and had no effect on stability, as demonstrated arthroscopically. In their series, Jakobsen11 has documented 19% Hill-Sachs lesions diagnosed on craniocaudal radiographs.
Glenoid Bone Lesions Two types of fractures occur involving the anterior inferior glenoid, the glenoid rim fracture and an avulsion fracture. The glenoid rim fracture is secondary to compression of the anterior inferior bony articulation of the glenoid by the humeral head (Fig. 20-6). Studies have shown an incidence of anterior glenoid rim fractures associated with an anterior dislocation ranging from 5.4% to 44%.22,23 However, we are unaware of any reports on the incidence of anterior glenoid rim fractures resulting from an initial first-time acute dislocation. Repeated episodes of instability create the inverted pear lesion as well as a typical bony Bankart lesion, and this is observed in the recurrent instability. Investigators in the past have recommended a coracoid transfer if the glenoid rim fracture comprises 25% of the anterior-posterior diameter of the glenoid. Lo24 commented on the containment of the humeral head by the glenoid as a result of two geometric variables. The first is the deepening effect of a wire glenoid caused by the longer arc of its concave surface; the second is the arc length of the glenoid itself. They cautioned that if the bony fragment is excised or if there is an inverted pear-shaped glenoid, arthroscopic techniques without a bone augmentation procedure may be predisposed to failure. The recognition and proper management of bone defects in the acute dislocation are important. In recurrent dislocations, increased failure rates with arthroscopic repair have been observed in the presence of bone loss.21,25,26
The pathoanatomy described pertains to the young athletic population. In athletes older than 50 years, Reeves27 has found capsular rupture, capsular detachment, and rotator cuff tear to be the predominant pathoanatomy after performing an arthrogram on postacute anterior dislocation patients. Most patients in Robinson’s study28 were middleaged. Of the seven isolated dislocations without a fracture, five had a massive rotator cuff tear; it was found that the presence of a rotator cuff tear is associated with a much higher risk of redislocation.
CAUSES AND EPIDEMIOLOGY For an anterior shoulder dislocation to occur, the mechanism of injury typically involves the position of abduction and external rotation, as seen in many contact sports. Studies have shown the incidence of traumatic shoulder instability in the general population to be approximately 1.7%. However, this can be doubled in those with high physical demands. In the United States Military Academy, the 1-year incidence was 2.8%, and 85% of instability events were caused by traumatic subluxation.29 After an anterior shoulder dislocation, the risk of recurrent shoulder instability is related primarily to the age at the time of dislocation. This is the single most important prognostic factor. There is a significantly higher rate of recurrent anterior shoulder instability in younger patients with acute traumatic anterior shoulder dislocations. Most recurrent instability episodes occur in the first 2 years after the primary incident. A study by McLaughlin and Cavallaro30 has found a 90% chance of recurrent instability in patients younger than 20 years, a 60% recurrence rate in patients 20 to 40 years of age, and a recurrence rate lower than 10% in patients older than 40 years. Hovelius31 published long-term rates of recurrent instability (at 10 years) and found a 66% risk of recurrent anterior instability for patients younger than 22 years, a 56% risk for patients aged 23 to 29 years, and a 20% risk for patients 30 to 40 years. More recently, at 2 years, Jakobsen11 found a 54% recurrence rate in patients treated conservatively after an initial anterior dislocation. There was a 3% recurrence in the group treated with open repair. Larrain32 reported a 5.1% recurrence in the acute instability group, with the events occurring during rugby. In the recurrent instability group, the recurrence rate was 8.3%. Postacchini33 reviewed patients 14 to 17 years of age and found that the recurrence rate after a primary traumatic dislocation is 92%; for adolescents with a Bankart lesion, they recommended prophylactic surgical stabilization at the time of initial injury.
Figure 20-6. Radiograph of a bony Bankart lesion.
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Activity level may also be an important factor when considering the risk of recurrence after an anterior dislocation. Arciero34 has shown that for first-time contact sport athletes, there is an 80% recurrence rate with conservative treatment and return to contact sports. Conversely, there is
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a 14% recurrence rate with arthroscopic treatment of the Bankart lesion and return to contact sports. In Hovelius’ series of Swedish hockey players, the redislocation rate was 90% in players older than 20 years, with a diminishing frequency with increasing age.35 Larrain36 found that most dislocations are in rugby players.
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conscious sedation or intra-articular local anesthetic. Miller39 reported the use of intra-articular lidocaine to facilitate reduction with the Stimson technique as a safe and effective method for treating acute shoulder dislocations in an emergency room. In this setting, it would be prudent first to obtain an x-ray (anteroposterior [AP], lateral, and axillary views) to confirm the direction of dislocation and to rule out associated fractures.
DIAGNOSIS Radiologic Features Evaluation and Physical Examination In the setting of an acute anterior shoulder dislocation in the athlete, the physician usually encounters the athlete on the field, in the training room, or in the emergency department (ED). Initial evaluation should focus on airway, breathing, and circulation to assess the overall stability of the patient. Once the patient is deemed stable, a detailed assessment of the injured extremity is conducted. If the physician is covering the game from the sidelines, he or she will witness the mechanism of the injury. The focused history should rule out associated injuries by asking about other symptomatic areas. In an acute first-time dislocation, the athlete will be in obvious discomfort and experiencing intense pain. The physical examination of the shoulder should follow a systematic approach to avoid missing concurrent pathology. It is important to perform pre- and postreduction neurovascular examinations. Nerve lesions include injury to the axillary nerve (most common), suprascapular nerve traction injury, and long thoracic nerve injury. Visser and colleagues38 have reported axillary nerve injury in 42% of anterior shoulder dislocations. Immediate recognition of an acute anterior dislocation is often possible because of the characteristic position of the athlete’s arm, which is held internally rotated against the body and supported by the contralateral arm. The athlete will resist any attempt to move the affected arm. Physical examination findings include the following: • Asymmetry of the deltoid contour. The affected side will demonstrate a sharp contour and a more prominent acromion when compared with the unaffected side. • The affected side may have a palpable fullness below the coracoid and toward the axilla. A closed reduction on the field or sideline or in training without first obtaining an x-ray is controversial. Many experienced physicians will perform a closed reduction on the field with the rationale that a reduction can be achieved before the onset of muscle spasms. This would allow a timely reduction, which would significantly reduce the level of pain without the need for conscious sedation. It is imperative that a repeat neurovascular examination be conducted postreduction. The other scenario is that the dislocation is not reduced on the field and the physician first sees the patient in the ED. By the time the patient arrives in the ED, a closed reduction is usually not possible without
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Radiographs should include a trauma series to document the direction of the dislocation and any associated fractures of structures such as the glenoid rim or greater tuberosity. A standard AP view of the arm in slight internal rotation is used to identify a fracture of the greater tuberosity. A true scapular AP radiograph permits evaluation of a glenoid fossa fracture, if present. In the office, after reduction, the West Point modified axillary view is used to assess bony avulsions of the attachment of the IGHL, bony Bankart lesions, or anterior-inferior glenoid deficiency.40 It is difficult to obtain this radiograph acutely because of guarding and pain but usually it can be obtained within several days. The Hill-Sachs lesion can be quantified and evaluated by examining the Stryker notch view. Computed Tomography A computed tomography (CT) scan can be an accurate means of determining glenoid version and overall glenoid morphology and, with three-dimensional reconstructions, provides an accurate assessment of any bone loss or size of rim fracture after an acute dislocation.41 Currently, the senior author uses CT to quantify the size of an anterior rim fracture after an acute dislocation (Fig. 20-7). Magnetic Resonance Imaging Magnetic resonance imaging (MRI) is used for the assessment of associated pathology. Contrast enhancement improves the diagnostic ability to detect labral tears (superior and anterior-inferior), rotator cuff tears (partialand full-thickness), and articular cartilage lesions. In the identification of HAGHL lesions, MRI scans in the midsagittal coronal oblique plane show the detachment of the inferior glenoid labrum (IGL) and reveal that the axillary pouch is converted from a fully distended U-shaped structure to a J-shaped structure as the IGL drops inferiorly (Fig. 20-8).42 This has been further defined in a follow-up study that describes the MRI appearance of a HAGHL lesion as an avulsion fracture from the neocortex in the humeral neck. The fluid-filled, distended, U-shaped axillary pouch is converted into a J-shaped structure by the extravasation of contrast material.19 Occasionally, with plain radiography, a thin, crescent-shaped calcific density is observed inferior to the anatomic neck of the humerus. The presence of this lesion may also be a relative contraindication to an arthroscopic shoulder stabilization procedure.
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and quality of life.36,37,43,44 On the contrary, Sachs found only half of his “high risk” contact or collision athletes requesting surgical stabilization during the follow-up period and concluded that early surgery should not be based on the presumption of future dislocations and disability.45 Patients 25 to 40 years have a much lower recurrence rate and rehabilitation after the dislocation is generally the best treatment. Patients older than 40 years who sustain an anterior dislocation have much lower recurrence rates in general (10% to 15%) but can have residual disability requiring priority treatment because of other soft tissue lesions, such as rotator cuff tear, nerve injury, and vascular injury.46
Nonoperative Treatment
Figure 20-7. Arthroscopic example of an inverted pear-shaped glenoid of the left shoulder, anterior-superior viewing portal, lateral posterior. Note the bony deficiencies of the anterior-inferior glenoid to the right.
TREATMENT Acute Anterior Instability Algorithm The decision for treatment in any patient after a dislocation should be individualized. In the case of a minor, it must involve the parent or legal guardian, and it must be remembered that choices always involve advantages and disadvantages. Once the diagnosis is made and the shoulder is reduced, the decision for subsequent treatment can be made. Age and activity levels are the most important factors guiding treatment. For the young athlete particularly involved in contact sports, 15 to 25 years, acute repair may be a viable option based on the high risk of recurrence, apprehension, and impact on sports participation
Traditional nonoperative treatment has included a period of immobilization with the arm in internal rotation. However, the length of immobilization, even up to 6 weeks, has not been found to reduce recurrence rates. In a long-term (10-year follow-up) study on immobilization outcomes after anterior shoulder dislocations by Hovelius,31 no effect on recurrence rates related to the length of immobilization was seen. Out of 247 primary anterior shoulder dislocators, 50% had a recurrent dislocation at 10 years. Of the recurrent dislocators, 50% had surgery and, of those with surgery, 50% were stable at 10-year follow-up. Interestingly, degenerative joint disease was found in surgical and nonsurgical candidates, with 11% of patients who underwent surgery having mild secondary degenerative joint disease at the 10-year follow-up.31 Recently, Itoi and colleagues47 have demonstrated with MRI better reapproximation of the Bankart lesion with the arm in 30 degrees of external rotation. A short-term clinical study has revealed decreased recurrence rates in patients immobilized in external rotation compared with those immobilized in internal rotation.47 Maintaining arm position in 30 degrees of external rotation for 3 to 4 weeks may make compliance with this treatment difficult for the young competitive athlete. The athlete who sustains a dislocation during a competitive season poses a unique clinical dilemma. Buss,48 in a review of athletes sustaining an anterior dislocation in season, has shown that a regimen of early range of motion and a shoulder brace restricting abduction and external rotation allowed 26 of 30 athletes to return and complete the season; 4 of 30 required in-season surgery. Many athletes coped with continued instability events during the season, and 16 additional athletes underwent surgical stabilization at the end of the season. Therefore, a total of 20 of 30 athletes underwent surgery within the first year after sustaining an acute anterior dislocation.
Figure 20-8. Magnetic resonance imaging (MRI) of lesions. MRI scan of humeral avulsion of the glenohumeral ligament (HAGHL) lesion.
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Although not proven, it can be hypothesized that with more dislocations or subluxations, more damage to the articular cartilage, bone, and capsule develops.49 It is our opinion that if an athlete has a second or third recurrence
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during the sport, then nonoperative management should be discontinued and surgical treatment options considered. Other at-risk periods for the athlete who sustains a firsttime dislocation are at the end of the season and spring training. The options are early mobilization, rehabilitation, and return to full activity. For the collision athlete, this is unpredictable. Another option is to immobilize the athlete in external rotation for 3 to 4 weeks, proceed with rehabilitation, and return to sports after 6 to 8 weeks. The experience of Itoi47 has suggested a reduced recurrence rate; however, further studies using this treatment regimen in young contact athletes are needed. In the young
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contact athlete, modern operative stabilization techniques (open and arthroscopic) reduce the recurrence rate from 80% to 90% to 3% to 15% and improve the quality of outcome.34,35,43,44 The algorithm presented in Figure 20-9 is a suggestion based on the literature and our experience. It should be used as a guide only.
Operative Treatment The rationale for acute repair is based on the following: (1) high recurrence rates in young athletic patients; (2) 87% to 100% incidence of acute capsulolabral avulsions
Primary traumatic anterior shoulder dislocation requiring reduction
Diagnostic workup: • X-rays • MRI arthrogram (to r/o HAGHL lesion)
In-season athlete Operative fixation Open/arthroscopic Bankart repair
Rehab
Immobilization Brace in external rotation
RTP in 6 months
RTP with brace (average 10 days); without brace when full strength and full ROM
RTP in 6 weeks
Recurrent anterior shoulder dislocations Doesn’t mind loss of time
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In-season athlete
Operative intervention
Conservative treatment Rehab and prophylactic brace: Sawa brace Duke Wyre brace
R/O bone lesion • X-ray: West Point, Stryker notch view • CT scan
Bone lesion
No bone lesion
Open Bankart repair PLUS capsulorraphy PLUS bone restoration procedure (e.g., Laterget, allograft, humeral head allograft)
Open or arthroscopic Bankart repair PLUS capsulorraphy
Figure 20-9. Decision-making algorithm for primary traumatic anterior shoulder dislocations. HAGHL, humeral avulsion of the glenohumeral ligament ; MRI, magnetic resonance imaging; ROM, range of motion; RTP, return to play.
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documented in clinical series that were amenable to repair; and (3) reversal of natural history and improved outcomes. In the operative repair of an acute dislocation, it is our preference to perform the repair within 2 weeks of the injury, taking advantage of the unique repair process and, in most cases, excellent capsulolabral tissue. The focus of the surgery is repair of the capsulolabral avulsion, usually with three suture anchors. With the introduction of high-strength suture material, retensioning of the inferior glenohumeral ligament is combined with repair of the Bankart lesion to address the stretch component of the ligament that occurs with the labral avulsion. Bigliani7 reported that with any type of capsular failure, there is a significant amount of elongation, suggesting that plastic deformation of the capsule has occurred. In the acute situation, an extensive capsular plication and routine closure of the rotator interval are not performed. Closure of the rotator interval is controversial and there are no clinical studies identifying the specific role of interval closure in the treatment of the shoulder instability. If the athlete has more than a 1⫹ sulcus sign with the arm in 30 degrees, or engages in a contact sport, we strongly consider rotator interval closure after acute repair of the capsulolabral lesion. Examination Under Anesthesia An examination under anesthesia (EUA) of both shoulders, in the supine position, is performed, documenting forward elevation, external and internal rotation with the arm at the side, and external and internal rotation with the arm abducted to 90 degrees. Anterior load and shift, posterior jerk, and sulcus tests are performed to assess instability. The EUA is used to confirm and add further information and assess for other pathology that may be present, not to make the diagnosis. When performing the load and shift test, care should be taken to compare both shoulders for the amount of humeral head translation. In addition, the amount of translation should be noted for each arm position with respect to the degree of humeral rotation and position of the arm in relation to the plane of the scapula. Arm rotation and position will influence the degree of translation because of their effects on changes in ligament length. Patient Position The lateral decubitus or beach chair position can be used for instability surgery. The beach chair position offers the advantage of being able to convert to an open procedure easily. When the beach chair position is used, a sterile arm holder is helpful for holding a desired arm position and for applying a distraction force to the arm. For the lateral decubitus position, a three-point distraction device (Arthrex, Naples, Fla) is used that allows longitudinal and vertical traction and enables the humeral head to
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be lifted reproducibly from the glenoid (Fig. 20-10A and B). A beanbag is used to stabilize the patient, with a hip holder also used just below the scapula posteriorly to stabilize the beanbag in case air is accidentally released. The patient is positioned in a 30-degree backward tilt, placing the glenoid in a parallel orientation to the floor. We frequently add a knee bump (see Fig. 20-10C) placed into the axilla, which provides improved exposure of the inferior aspect of the joint. In most cases, general endotracheal intubation is used for anesthesia, with an interscalene block for pain control. The beach chair position is amenable only to an interscalene block for the procedure; because of the uncomfortable nature of the lateral position, we advocate general anesthesia with or without regional block. Preoperative antibiotics are administered intravenously before skin incision. Portal Placement A standard posterior portal should be placed slightly more laterally than the joint line. If the portal is placed medially to the joint line, this will require the surgeon to lever the arthroscope against the glenoid, making the stabilization procedure difficult. An 8- to 10-mm incision is made, and the blunt arthroscope sheath and trocar are inserted atraumatically into the space between the glenoid rim and humeral head. The anterior portals are then made using spinal needles for localization. The first anterior portal made is superior in the rotator interval, as high in the anterior superior quadrant of the shoulder as possible, while still allowing the cannula to be placed anterior to the biceps tendon. On the outside of the shoulder, this portal is closer to the anterior acromion. Medial placement of the cannula will compromise access to the glenoid. In general, a 7- ⫻ 7-cm cannula, smooth or ridged, is placed for suture shuttling. The second portal is the anterior inferior portal.Because of the instruments used through this portal, it usually requires an 8.25- ⫻ 7-cm cannula. Two different anterior inferior portals can be placed. The primary anterior inferior portal is made at the superior rolled edge of the subscapularis and angled inferiorly. Once again, this is also made with spinal needle localization but avoids the trauma of going through the subscapularis tendon. In viewing the portal placement from the outside, the spinal needle is generally placed just lateral to the coracoid process. This portal is typically used to place anchors along the anteroinferior glenoid. In most cases, the anterosuperior and anteroinferior portals are sufficient to perform the repair. Occasionally, the anteroinferior portal is not adequately positioned to gain access to the anteroinferior glenoid rim for anchor placement. The solution for this is a trans-subscapular portal initially established by placing an 18-gauge spinal needle through
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the subscapularis muscle. This is usually slightly inferior to the traditional anteroinferior portal. A percutaneous incision is made, followed by blunt spreading using a hemostat to the joint level. A small-diameter trocar can be placed and permits drilling and anchor placement at the 5-o’clock position (Fig. 20-11).
A 30°
A
B
B
C Figure 20-10. Traction device. A, Lateral position traction device (Arthrex, Naples, Fla). B, Positioning of the patient with the lateral traction device and a 30-degree posterior tilt. C, Knee bump placed into the axilla.
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C Figure 20-11. Inferior anchor placement. A, Percutaneous 18-gauge needle used to set up trans-subscapular portal. B, Outside view of 3-mm trocar through subscapularis. C, Arthroscopic view of trocar for placement of drill at the 5-o’clock position on the glenoid rim.
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We recognize that there are many individual preferences to performing a repair with regard to portal placement and positioning of the arthroscope and instrumentation. Many surgeons prefer to keep the arthroscope posterior and work through the anterosuperior and anteroinferior portals. Some surgeons prefer visualization for most of the procedure, with the arthroscope in the anterosuperior portal and instrumentation from the anteroinferior and posterior portals. The surgeon should be comfortable with changing portals to improve access and adjust to any condition encountered, which improves the technical performance of the procedure. Fluid management is also important. Shoulder overdistention is compounded by improper portal development and a lengthy procedure. It is always important to establish accurate and small portals, use cannulas at all times to create a seal in the glenohumeral joint, and monitor the amount of fluid pressure to decrease the amount of fluid extravasation. An ideal pressure to perform arthroscopic stabilization has not been reported. However, analysis and evaluation of pressure and shoulder distention as the procedure progresses are critical. Bankart Repair With Suture Anchors Repair of the Bankart lesion is the critical step in this procedure. The suture anchor repair with arthroscopic knot tying is similar to the open repair technique and is extremely versatile and reproducible. Although arthroscopic repair has been performed with transglenoid suturing, bioabsorbable tacks, and knotless devices, we favor the suture anchor technique because it most closely resembles the open technique, which has a long history of satisfactory results. There are two variations of this technique, the suture-first and anchor-first methods. Clinically there have been no reported differences between any of these techniques in the literature and their use is based on surgeon preference. The anchors themselves can be metal or bioabsorbable. No differences have been reported clinically based on the material of the anchor. We recommend bioabsorbable anchors because most instability patients are young, and we attempt to avoid the theoretical possibility of migration. Proper anchor placement is the most critical step and no material can help an improperly placed anchor. Anchor-First Technique. The anchor first technique involves placing an anchor through the anterior inferior cannula first, and then shuttling the suture limb. At this time, it is important to note the position of the anterior inferior cannula and the position in which the anchor should be placed into the glenoid. Occasionally, the position of the cannula is appropriate for suture shuttling but not for placement of the anchor. In this case, a percutaneous approach can be used to insert an anchor into the glenoid at the 5-o’clock position. The advantage of this technique allows a more appropriate perpendicular
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placement of the anchor into the glenoid face at approximately 2 to 3 mm over the articular service without bubbling or causing articular injury. After the anchor has been successfully inserted, one of the suture limbs is passed out of the anterior superior cannula. This limb, if using a metal anchor or anchor with a fixed eyelet, is the limb on the tissue side of the suture. The eyelet should be perpendicular to the labrum. A tissue penetrator or suture-shuttling device is used to pass a suture into the tissue inferior to the anchor. The end of the suture is then grasped and pulled out through the anterior superior cannula. A small square knot is tied in the passing suture, serving as a dilating knot. This is followed by tying the nonabsorbable braided suture to the monofilament suture line further distally and pulling the passing stitch through the anterior inferior cannula—hence, shuttling the suture through the labrum, inferior-glenoid ligament, and scapular periosteal complex. On tightening this suture with proper arthroscopic knottying technique, a shift of tissue from inferior to superior should be observed. If the tissue bite was not placed inferior enough to the anchor, this step should be repeated before continuing the operation. To tie the knot, the knot pusher is placed on the suture limb that is on the tissue side. This will be the post. A sliding locking knot or a nonsliding knot (multiple half-hitches) can be tied at this time. It has been determined that after placement of a sliding knot or multiple half-hitches, three alternating half-hitches while switching the post is the most secure final fixation.50 The knot should end up on the tissue side so that the labrum can create a bumper effect. The next two or three anchors are then placed approximately 5 to 7 mm apart from each other in the same fashion as described. On completion of the procedure, a bumper should be observed at the anterior inferior glenoid between the 3- and 6-o’clock positions. Suture-First Technique. The suture first-technique, which is our preference, involves placing a suture-passing device initially to ensure adequate soft tissue shift, followed by placement of the anchor. A suture-passing device is initially placed through the anterior inferior cannula. The capsular tissue is pierced about 5 to 7 mm laterally to the labrum as close to the 6-o’clock position as possible and the labrum is pierced slightly more cephalad. The passing suture is passed through the tissue and shuttled through the posterior portal; the arthroscope is in the anterosuperior portal (Fig. 20-12). The shuttling suture or device is now in the anteroinferior and posterior portals. Tension is placed on this suture to observe the amount of shift that can be accomplished by placing the anchor at the appropriate position. If it is determined that this suture is not inferior enough, this suture can be used as a traction suture and a second suture can be placed more inferiorly.
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Figure 20-12. Arthroscopic view of the right shoulder viewed from anterosuperior portal. The shuttle suture is placed through the capsule and labrum near the 6-o’clock position.
When an appropriate amount of tissue tension is established, the anchor is placed through the anterior inferior portal and onto the glenoid rim slightly more cephalad than the passing suture. For example, for a right shoulder, the passing suture should be placed at the 5:30- or 6-o’clock position and the anchor at the 5-o’clock position (Fig. 20-13). As noted, once the anchor is placed, the two limbs of the suture are separated, one through the anterior superior cannula and the other shuttled through the tissue. Because of the cephalad positioning of the anchor relative to the shuttling suture, when the nonabsorbable suture is shuttled and then tied, the labrum is repaired and there is retensioning of the inferior glenohumeral ligament with each anchor (Fig. 20-14). The same steps are repeated two or three times, depending on the repair quality and amount of injury (Fig. 20-15).
Figure 20-13. Arthroscopic view of the right shoulder depicting shuttling suture inferior to anchor placed at about the 5-o’clock position.
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Figure 20-14. Knot tying. With this technique, the capsule and labrum can be retensioned in a cephalic position.
Rotator Interval Closure The rotator interval is an important anatomic region with respect to anterior shoulder stability. This anatomic region is defined as the articular capsule bounded superiorly by the anterior portion of the supraspinatus tendon, inferiorly by the superior portion of the subscapularis tendon, medially by the base of the coracoid process, and laterally by the long head of the biceps tendon. The capsular tissue is reinforced by the coracohumeral ligament (CHL) and superior glenohumeral ligament (SGHL). The rotator interval is of varying size and is present in the fetus as well as in the adult. Harryman51 demonstrated that sectioning the rotator interval in cadaveric specimens results in increased glenohumeral translation in all planes tested. Imbrication of rotator interval lesions results in
Figure 20-15. Completed repair.
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decreased posterior and inferior glenohumeral translation when compared with the intact state. Field52 reported good or excellent results in 15 patients who underwent surgical repair of isolated rotator interval defects. There is no consensus regarding the indications for rotator interval closure. In the acute, first-time dislocation, we are cautious of routine performance of this procedure because of concerns of postoperative stiffness. During operative stabilization after a primary dislocation, we currently use this adjunct for the collision athlete and the athlete with a 1⫹ sulcus that is not reduced with the arm in 30 degrees of external rotation Many surgeons have reported techniques for closing the rotator interval. One involves removing the anterior inferior cannula and placing all instrumentation through the anterior superior cannula. We prefer using an absorbable suture for the closure. The middle glenohumeral ligament (MGHL), a small portion of the subscapularis tendon, or both, is pierced with a spinal needle or sutureshuttling device and a monofilament suture is deployed (Fig. 20-16A). The SGHL-CHL complex is pierced with a penetrator and the monofilament suture is grasped (see Fig. 20-16B). This tissue then can be tied through a cannula internally or externally and cut with a guillotine knot cutter (see Fig. 20-16C). Special Pathoanatomic Variants Extension of Anterior Inferior Labrum Tear Into Superior Labrum. If the labral tear extends from the anterior inferior glenoid up into the superior labrum, the same anterior cannula can be used to continue placing suture anchors. We recommend two or three suture anchors for superior labrum tears, with one placed in front of the biceps tendon anchor and one or two placed behind the biceps tendon anchor, depending on the amount of biceps instability. The anchor is placed in front of the biceps tendon anchor and guided through the anterior superior cannula. The one or two anchors placed posteriorly to the biceps anchor can be placed percutaneously via the Port of Wilmington portal.53 This portal is 1 cm lateral and 1 cm anterior to the posterior lateral corner of the acromion, through the musculotendinous junction of the rotator cuff. Extension of Capsulolabral Injury Posteriorly. In some cases, the lesion may involve the posterior labrum, necessitating placement of anchors and repair along the posteroinferior glenoid. To have appropriate access to the posteroinferior glenoid and avoid iatrogenic injury to the articular surface, an accessory posteroinferior portal is required. This portal is made roughly 2 cm lateral and 1 cm inferior to the standard posterior portal. An 18-gauge spinal needle is used under direct visualization to assess the position and an 8.25- ⫻ 9-cm cannula is then placed. This portal results in accurate posteroinferior anchor insertion, because the arthroscope is kept in the anterosuperior portal and suture-shuttling devices are used in the posterior and anteroinferior portals (Fig. 20-17).
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A
B
C Figure 20-16. Closing the rotator interval. A, Suture-shuttling device through the middle glenohumeral ligament placing a monofilament suture into the joint. B, Tissue penetrator through the superior glenohumeral ligament and coracohumeral ligament retrieving a monofilament suture. C, Rotator interval is closed extra-articularly.
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Acute Osseous Bankart Lesions. Acute osseous Bankart lesions can be repaired according to Sugaya’s technique.54 An arthroscopic evaluation is first conducted. Viewing from the anterior portal helps confirm the osseous glenoid defect in the anteroinferior quadrant. Mobilization of the labroligamentous complex and the osseous fragment from the glenoid neck needs to be performed carefully, followed by repair of the inferior labrum adjacent to the osseous fragment. Bony fragment fixation can be achieved by different methods, such as passing the suture through or around the fragment. Suture anchors are then used to reconstruct the entire labroligamentous complex.
A
POSTOPERATIVE CARE The biologic healing response of the repaired and imbricated tissue must be respected. One observation that may have led to some of the earlier arthroscopic failures for anterior instability is that, because of the significant reduction in postoperative pain, these patients want to move their shoulders earlier, imparting more stress to the repair site. This early cyclic stress and motion eventually fatigue the plication stitches and cause a failure of the repair. The first goal to postoperative success is maintenance of anterior-inferior stability. The second goal is the restoration of adequate motion—specifically, external rotation. The third is a successful return to sports or physical activities of daily living in a reasonable amount of time.
B
C Figure 20-17. Creating an accessory posteroinferior portal. A, Outside image of an 18-gauge needle used to guide placement of posteroinferior anchor. B, Arthroscopic image of an 18-gauge needle in proper trajectory to drill into posteroinferior glenoid. C, Arthroscopic image of posteroinferior trocar.
Our protocol for anterior-inferior shoulder instability treated by arthroscopic means involves postoperative immobilization immediately in an abduction arthrosis. This allows the arm to be fixed in a slight amount of external rotation. Codman’s exercises, combined with pendulum exercises, are started immediately. Active-assisted rangeof-motion, external rotation (0 to 30 degrees), and forward elevation (0 to 90 degrees) exercises are also started at this time. This regimen is maintained for the first 6 weeks. The use of cold therapy devices has been successful in reducing postoperative pain. From weeks 6 to 12, activeassisted as well as active range-of-motion exercises are started, with the goal of establishing full range of motion. No strengthening exercises or any type of repetitive exercises are started until after full range of motion has been established. This protocol is based on tendon to bone healing in a dog model.55 Early resistance exercises with aggressive early postoperative rehabilitation do not appear to offer substantial advantages and could compromise the repair. Strengthening is begun once there is full, painless, active range of motion. Strengthening is begun at 12 weeks, with sports-specific exercises started at 16 to 20 weeks. Final
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contact athletic training is started between 20 and 24 weeks postoperatively. Pagnani and Dome56 have reported on open stabilization in American football players. Their postoperative program is similar to the one described here. At 0 to 4 weeks, the arm is immobilized with a sling and internal rotation and double range-of-motion and pendulum exercises are begun. From 4 to 8 weeks, passive- and active-assisted shoulder range-of-motion exercises with external rotation limited to 45 degrees are initiated. Rotator cuff strengthening and internal and external rotation strengthening with the arm at low abduction angles are begun when 140 degrees of active forward elevation has been achieved. From 8 to 12 weeks, deltoid isometric exercises with the arm in low abduction angles and body blade exercises are started. Abduction is slowly increased during rotator cuff and deltoid-strengthening exercises. In addition, scapular stabilizer strengthening and horizontal abduction exercises are also begun. From 12 to 16 weeks, restoration of terminal external rotation is achieved. Proprioceptive neuromuscular feedback patterns are used, and plyometric and sports-specific motion exercises using pulley, wand, or manual resistance, are begun. After 16 weeks, conventional weight training is started and rehabilitation is orientated toward return to sports, progressing from field drills to contact drills. An abduction harness can be used for select football positions, such as linemen. Full contact sports are instituted when abduction and external rotation strength are symmetrical on manual muscle testing, typically 4 to 5 months postoperatively.
TECHNICAL ERRORS For successful treatment of arthroscopic anterior-inferior instability, adequate visualization is imperative. The lateral decubitus position with a traction device can provide vertical distraction, enabling the humeral head to float superiorly, and horizontal distraction, pulling the humeral head inferiorly. Traction allows the surgical team to work unencumbered by not having to hold the arm. If adequate visualization of the anterior inferior glenoid and pathology cannot be established, an open procedure is recommended.
lateral position will force the arthroscope to be placed at an angle at which it has to look over the posterior glenoid, which makes the following procedures more difficult. If the surgeon finds that she or he has to look over the top of the glenoid, a new posterior-inferior portal should be established immediately. If the surgeon is worried about extravasation of fluid into the posterior compartment, or if the fluid dynamics is altered by making a second portal posteriorly, a nonfunctional cannula can be placed into the first portal. This will seal off potential extravasation of fluid. When establishing the anterior portals, two important concepts must be observed. The first is that the two cannulas should be separated as far from each other as possible, internally and externally. This allows for easier passage when shuttling sutures. The second is to ensure that the anteriorsuperior portal is not placed into the posterior aspect of the biceps. If this does occur, care must be taken not to lock the proximal biceps tendon in the suture loop.
Suture Anchors Suture anchor placement should be 2 to 3 mm from the articular margin. Visualization should be maintained as the anchor is inserted. Improper angle of anchor insertion can cause articular surface damage or inadequate bone placement, allowing anchor migration and possible articular cartilage damage (Fig. 20-18). Two types of anchors are available, metal or bioabsorbable. Each has its advantages and disadvantages. Metal anchors generally can be inserted without taping after drilling or punching, eliminating a potential step during insertion. Also, they are mechanically stronger, with infrequent physical anchor breakage. In long-term follow-up, the anchor or cartilage may subside and there may be erosion of the metal anchor on the articular surface.
Incorrect Portal Placement Portal placement is critical to adequate visualization and execution of an arthroscopic anterior inferior stabilization procedure using capsular plication and suture anchors. In the lateral position, to establish the posterior portal, it is important to err slightly more laterally than normal. A direct entrance from the posterior skin through the infraspinatus muscle and capsule is ideal but, if an error is going to be made or if the patient is large, the portal should be placed more laterally. Medial portal placement in the
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Figure 20-18. Improper anchor placement. Intra-articular metal is exposed and there is articular damage to the humeral head.
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Bioabsorbable anchors have the advantage of being incorporated into the body over time, but have the disadvantage of causing varying degrees of tissue reaction. They generally require tapping, which is an additional step. This can lead to anchor-hole mismatch, which may cause anchor fracture. The advantage of the bioabsorbable anchor at this point is that a second anchor then can be placed right on top of the first anchor by retapping or drilling the original hole should this be necessary. Bioabsorbable anchors, such as BioFastak and BioSutureTak (Arthrex, Naples, Fla), also have the advantage of having a suture loop placed inside them, in which a suture is embedded into the bioabsorbable anchor. This allows for consistent sliding of different types of sutures.
Suture Shuttling and Knot Tying Passing the suture through the tissue can be frustrating. It is important to ensure that the suture shuttled through the tissue is inferior to the anchor, allowing a superior shift of tissue. This can be done directly with a sharp penetrator, which pierces the tissue, grabs the sutures, and then pulls them out, or indirectly by a suture shuttle system, in which a suture-passing device passes a monofilament suture into the tissue. This is retrieved through a cannula and the suture to be shuttled through is then tied to this and brought back through the tissue. Tangling and confusion of the sutures can occur at this time, and it is important to be methodical. Unloading of the anchor can also occur during suture shuttling. To prevent this, the arthroscope should visualize the anchor directly. If both limbs of the suture are seen moving, then the anchor is being unloaded. This is satisfactory initially as the loop is pulled out through the cannula. However, once the loop is out of the cannula, special attention should be paid so that no further suture is removed from the anchor. Because it may be difficult to determine which limb will unload the anchor, look at the anchor and pull on one limb of the suture. If there is no further movement of the suture through the anchor, this is the free limb, which can be pulled through the cannula without further concern. For further safety, a hemostat can be placed on the limb that is not sutured, so that it cannot be pulled through the cannula. Although at times time-consuming and cumbersome, these small checks can prevent the unfortunate complication of unloading an anchor. If sutures do become tangled intraarticularly (Fig. 20-19), the suture should be withdrawn from the joint and untied, and the process started from the beginning. If there is not enough room or suture length, a second suture can be tied to the end of the tangled suture; this can be pulled through, allowing more length of the suture to be untied outside the cannula and then easily brought back in through the anchor. There are two classifications of knots that can be tied, sliding and nonsliding knots. We will not describe the different knots available here, but it is important to realize that this is a potential area of difficulty if the knot prematurely locks
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Figure 20-19. Example of suture tangled in the shoulder.
or there is neither knot nor loop security. After tying the initial throw, it is important to observe whether all excess suture has been taken out of the system and whether the knots and loops are indenting the tissue. If this has not been achieved, the knots should not be locked until this is observed. To avoid twisting of the sutures and loose knots, the knot pusher can be placed on one of the limbs. This is then slid down and, if there is a twist, can be untwisted at this time. Any other abnormalities in the suture can be observed. If a knot prematurely locks or if it is tied and is not securing the tissue adequately, a second anchor and suture must be placed as close to the original knot as possible. A loose knot will never get stronger over time.
Postoperative Glenohumeral Noise This is an inconsistent physical examination finding that occasionally plagues the postoperative course. Normally, there is synovialization of the sutures (Fig. 20-20). If this does not happen, a squeak can be detected that may necessitate removal of the knot after healing has been established.
OUTCOMES Many studies have reported improved outcomes following acute arthroscopic repair. In one prospective randomized trial,44 arthroscopic repair not only decreased recurrence rates, but also resulted in improved quality of life. Other surgeons have reported improved outcomes following acute arthroscopic repair, as measured by SF-36 and Rowe scores.36,43,57 Most recently, Jakobsen and associates11 have reported on the 10-year outcome of primary open repair versus nonoperative treatment for primary anterior dislocation. At 10 years, the surgical group had
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Figure 20-20. Example of arthroscopic labral repair 3 weeks post op. This shoulder underwent arthroscopy for squeak secondary to the prominent suture.
75% good or excellent results and the nonoperative group had 75% unsatisfactory results secondary to pain, apprehension, or recurrent instability. In addition, in the nonoperative group (even the patients who did not experience recurrent dislocation), 39% had limitation of activity and positive apprehension. Furthermore, this study has demonstrated that patients initially treated nonoperatively, who then required surgical stabilization, have inferior results compared with those stabilized primarily. Therefore, it can be concluded that acute arthroscopic repair for the athlete with a first-time traumatic anterior dislocation leads to improved outcomes. The decision needs to be made in conjunction with the patient and family. The timing of the season also needs to be considered. If the dislocation occurs during the season, consideration should be given to nonoperative management to help the athlete complete the season. A thorough discussion with the patient regarding surgical stabilization after the season should also be undertaken.
References 1. Matsen FA, Thomas SC, Rockwood CA, Wirth MA: Glenohumeral instability. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed, vol 2. Philadelphia, WB Saunders, 1998, pp 633-639. 2. Lephart SM, Warner JP, Borsa PA, Fu FH: Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulder. J Shoulder Elbow Surg 3:371-379, 1994. 3. Turkel SJ, Panio MW, Marshall JL: Stabilizing mechanism preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 4. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990.
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5. Howell SM, Galinat BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop Relat Res (243): 122-125, 1989. 6. Lazarus MD, Sidles JA, Harryman DT 2nd, Matsen FA 3rd: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 7. Bigliani LU, Pollock RG, Soslowsky U, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 8. Baker CL, JW Uribe JW, Whitman C: Arthroscopic evaluation of acute initial anterior shoulder dislocations, Am J Sports Med 18:25-28, 1990. 9. Norlin R: Intraarticular pathology in acute, first-time anterior shoulder dislocation: An arthroscopic study. Arthroscopy 9:546-549, 1993. 10. Taylor DC, Arciero RA: Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med 25:306-311, 1997. 11. Jakobsen BW, Johannsen HV, Suder P, Sojbjerg JO: Primary repair versus conservative treatment of first-time traumatic anterior dislocation of the shoulder: A randomized study with 10-year follow-up. Arthroscopy 23:118-123, 2007. 12. Neviaser TJ: The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior instability of the shoulder. Arthroscopy 9:17-21, 1993. 13. Arciero RA, Taylor DC, Snyder RJ, et al: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 14. Savoie FH, Field LD, Atchinson S: Anterior superior instability with rotator cuff tearing: SLAC lesion. Oper Tech Sports Med 8:221-224, 2000. 15. Nicola T: Anterior dislocation of the shoulder. J Bone Joint Surg 26:619-616, 1941. 16. Richards DP, Burkhart SS: Arthroscopic humeral avulsion of the glenohumeral ligaments (HAGHL) repair. Arthroscopy 20(Suppl 2):134-141, 2004. 17. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of shoulder instability. Arthroscopy 11:600-607, 1995. 18. Bokor DC, Conboy VB, Olsen C: Anterior instability of the glenohumeral joint with humeral avulsion of the glenohumeral ligament: A review of 41 cases. J Bone Joint Surg Br 81:93-96, 1999. 19. Bui-Mansfield LT, Taylor DC, Uhorchak JM, Tenuta JJ: Humeral avulsions of the glenohumeral ligament: Imaging features and a review of the literature. AJR Am J Roentgenol 179:649-655, 2002. 20. Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863-873, 1981. 21. Burkhart SS, De Beer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677-694, 2000. 22. Scheibel M, Magosch P, Lichtenberg S, Habermeyer P: Open reconstruction of anterior glenoid rim fractures. Knee Surg Sports Traumatol Arthrosc 12:568-573, 2004. 23. Bigliani LU, Newton PM, Steinmann SP, et al: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med 26:41-45, 1998.
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24. Lo IK, Parten PN, Burkhart SS: The inverted pear: An indicator of significant bone loss. Arthroscopy 20:169-174, 2004. 25. Tauber M, Resch H, Forstner R, et al: Reasons for failure after surgical repair of anterior shoulder instability. J Shoulder Elbow Surg 13:279-285, 2004. 26. Boileau P, Villalba M, Héry JY, et al: Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am 88:1755-1763, 2006. 27. Reeves B: Arthrography of the shoulder. J Bone Joint Surg Br 48:424-435, 1966. 28. Robinson CM, Kelly M, Wakefield AE: Redislocation of the shoulder during the first six weeks after a primary anterior dislocation: Risk factors and results of treatment. J Bone Joint Surg Am 84:1552-1559, 2002. 29. Owens BD, Duffey ML, Nelson BJ, et al: The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med 35:1168-1173, 2007. 30. McLaughlin HL, Cavallaro WU: Primary anterior dislocation of the shoulder. Am J Surg 80:615-621, 1950. 31. Hovelius L, Augustini BG, Fredin H, et al: Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am 78:1677-1684, 1996. 32. Larrain MV, Montenegro HJ, Mauas DM, et al: Arthroscopic management of traumatic anterior shoulder instability in collision athletes: Analysis of 204 cases with a 4- to 9-year follow-up and results with the suture anchor technique. Arthroscopy 22:1283-1289, 2006. 33. Postacchini F, Gumina S, Cinotti G: Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg 9:470-474, 2000. 34. Arciero RA, Wheeler JH, Ryan ID, et al: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med 22: 589-594, 1994. 35. Hovelius L: Shoulder dislocation in Swedish ice hockey players. Am J Sports Med 6:373-377, 1978. 36. Larrain MV, Botto GJ, Montenegro HJ, Mauas DM: Arthroscopic repair of acute traumatic anterior shoulder dislocation in young athletes. Arthroscopy 17:373-377, 2001. 37. Law BK, Yung PS, Ho EP, et al: The surgical outcome of immediate arthroscopic Bankart repair for the first time anterior shoulder dislocation in young active patients. Knee Surg Sports Traumatol Arthrosc 16:188-193, 2008. 38. Visser CP, Coene LN, Brand R, Tavy DL: The incidence of nerve injury in anterior dislocation of the shoulder and its influence on functional recovery. A prospective clinical and EMG Study. J Bone Joint Surg Br 81:679-685, 1999. 39. Miller SL, Cleeman E, Auerbach J, Flatow EL: Comparison of intra-articular lidocaine and intravenous sedation for reduction of shoulder dislocations: A randomized, prospective study. J Bone Joint Surg Am 84:2135-2139, 2002. 40. Rokous JR, Feagin JA, Abbott HG: Modified axillary roentgenogram. A useful adjunct in the diagnosis of recurrent instability of the shoulder. Clin Orthop Relat Res 82:84-86, 1972. 41. Sugaya H, Moriishi J, Dohi M, et al: Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am 85:878-884, 2003. 42. Stoller DW: MR arthrography of the glenohumeral joint. Radiol Clin North Am 35:97-116, 1997.
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43. Bottoni CR, Wilckens JH, DeBerardino TM, et al: A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med 30:576-580, 2002. 44. Kirkley A, Werstine R, Ratjek A, Griffin S: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 21:55-63, 2005. 45. Sachs RA, Lin D, Stone ML, et al: Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am 89:1665-1674, 2007. 46. Simank HG, Dauer G, Schneider S, Loew M: Incidence of rotator cuff tears in shoulder dislocations and results of therapy in older patients. Arch Orthop Trauma Surg 126:235-240, 2006. 47. Itoi E, Hatakeyama Y, Sato T, et al: Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence. A randomized controlled trial. J Bone Joint Surg Am 89:2124-2131, 2007. 48. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32:1430-1433, 2004. 49. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment: Incidence and contributing factors. Am J Sports Med 32:1165-1172, 2004. 50. Lo IK, Burkhart SS: Biomechanical principles of arthroscopic repair of the rotator cuff. Operat Tech Orthop 12:152-153, 2002. 51. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992. 52. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557-563, 1995. 53. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 54. Sugaya H, Moriishi J, Kanisawa I, Tsuchiya A: Arthroscopic osseous Bankart repair for chronic recurrent traumatic anterior glenohumeral instability. J Bone Joint Surg Am 87: 1752-1760, 2005. 55. Rodeo SA, Arroczhy SP, Tobilli PA, et al: Tendon healing in a bone tunnel: A biomechanical and histological study in the dog. J Bone Joint Surg Am 75:1795-1803, 1993. 56. Pagnani MJ, Dome DC: Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am 84:711-715, 2002. 57. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM: Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med 29:586-592, 2001.
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CHAPTER 21 Bankart Lesions: Diagnosis
and Treatment with Arthroscopic and Open Approaches J.R. Rudzki and David W. Altchek
As the instrumentation and techniques for arthroscopic stabilization and capsulolabral reconstructive procedures continue to improve, the debate over the optimal surgical approach for operative management of the Bankart lesion persists. First described in 1938, the Bankart lesion is a detachment of the anteroinferior labrum,1 which in conjunction with a concomitant capsular injury2 may result in anterior or anteroinferior glenohumeral instability (Fig. 21-1). Anatomic surgical reconstructions for this injury pattern include the classic Bankart repair described by Rowe and colleagues in 1978,3 with or without the capsular shift procedure described by Neer and associates in 1980.4 Several modifications of these open techniques were subsequently described,5-8 with a high rate of good to excellent results; this led some surgeons to declare open surgical treatment of the Bankart lesion the gold standard as the era of arthroscopic anterior stabilization began. The debate over optimal treatment of Bankart lesions and anterior instability continues today, at a time when arthroscopic techniques and instrumentation have rapidly and dramatically transformed these surgical procedures. Anterior and multidirectional instability is addressed in Chapters 17 and 19. This chapter will focus on the diagnosis and treatment of Bankart lesions with arthroscopic and open techniques through an examination of anatomy and pathophysiology, as well as the biomechanical and clinical outcomes data presented in the literature. Limitations of the available literature and opportunities for future research will be discussed in the context of clinical relevance.
tissue Bankart lesions, capsular injury and laxity, Hill-Sachs lesions, and concomitant injuries to the superior labral anterior-posterior (SLAP) and posterior aspects of the glenoid labrum. Less common but important injuries to recognize include superior rotator cuff and subscapularis injuries, glenoid fractures with bony compromise, humeral avulsion of the glenohumeral ligament (HAGHL) lesions, and glenoid dysplasia. Bankart lesions have been reported in 65% to 97% of patients who undergo surgical treatment for anterior instability.3,19-21 Fracture or injury to the glenoid rim has been reported in up to 73%, Hill-Sachs lesions have been reported in up to 90%, rotator cuff tears in up to 13%, and SLAP or posterior labral tears in 10% of cases.3,11,20 The Bankart lesion is an avulsion of the anteroinferior labrum (Fig. 21-2), which in conjunction with a concomitant capsular injury2 may result in anterior or anteroinferior glenohumeral instability. Bony Bankart lesions refer to those situations in which a portion of the adjacent anteroinferior aspect of the glenoid has fractured. These fragments typically remain attached to the avulsed labral and capsular tissue and may alter the normal geometry and surface area of the glenoid.22,23 This is clinically relevant because anterior glenoid rim fractures are a known cause of recurrent anterior shoulder instability.22,24-26 In discussing post-traumatic alterations of normal glenoid and humeral head osseous geometry, the concept of articular arc deficit as popularized by Burkhart and DeBeer23 is useful. Loss of bone from the anteroinferior aspect of the glenoid may result in what they have termed the inverted-pear glenoid, which has significant implications for choice of operative approach and long-term prognosis. In a study of 194 consecutive arthroscopic Bankart repairs, they reported a 4% recurrence rate in patients without significant bone defects (articular arc disruption) in comparison with a 67% recurrence rate for patients with significant bone defects and for contact athletes, and an increase in recurrence rate from 6.5% to 89% for patients without and with significant bone defects, respectively.
PATHOANATOMY A thorough understanding of the pathoanatomy involved in the diagnosis and treatment of Bankart lesions is essential for their treatment.9,10 The importance of this knowledge is emphasized by the literature, which supports the concept that there is no one essential lesion responsible for recurrent anterior shoulder instability.2,11-19 A recognition of the implications of common injury patterns and subtle findings help direct treatment intra-operatively in cases with multiple factors involved (e.g., symptomatic laxity versus instability). Typical pathoanatomy encountered in the treatment of anterior instability includes bony and soft
The Hill-Sachs lesion is an osteochondral impaction fracture involving the posterosuperior aspect of the humeral head (Fig. 21-3).27 It results from an impaction of the subchondral bone of the posterolateral aspect of the humeral 257
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Glenoid HH
Glenoid
C L C
L a b r u m
AIGHL Humeral head
A Figure 21-1. Bankart lesion in a left shoulder. This lesion is viewed from the posterior portal. CLC, capsulolabral complex; HH, humeral head.
head on the anterior aspect of the glenoid as the humeral head dislocates anteriorly. There are two types of Hill-Sachs lesions with which the surgeon must be familiar, the engaging and nonengaging forms. Just as a glenoid bone deficit may impair stability of the glenohumeral articular arc, the Hill-Sachs lesion may compromise glenohumeral stability and is an important potential cause of recurrent anterior shoulder instability. The presence of a large Hill-Sachs lesion has been reported in one study to double the recurrence rate of anterior instability after Bankart repair20 and has otherwise been reported to carry a statistically significant worse prognosis with regard to recurrent instability.28 The most common type of Hill-Sachs lesion is the nonengaging lesion, which does not mechanically interact with the anterior corner of the glenoid; therefore, by itself, it is not a significant threat for recurrent instability.
LITERATURE REVIEW Basic Science Familiarity with the clinical pathoanatomy encountered in the treatment of Bankart lesions is greatly enhanced through a knowledge of the relevant basic science data that support the clinical observations and associations reported in the literature. Several studies have improved our understanding of the multiple factors involved in recurrent instability and greatly assist the surgeon in patient and procedure selection for arthroscopic and open treatment of Bankart lesions. As noted, cadaveric studies have suggested that an isolated Bankart lesion may not be sufficient to cause abnormal glenohumeral translation or recurrent anterior
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HH
AIGHL G
B Figure 21-2. Bankart lesion. A, Bankart lesion in a right shoulder with identification of the AIGHL (anterior band of the inferior glenohumeral ligament). B, Arthroscopic image demonstrating attenuation of the AIGHL in a left shoulder.
instability.2,11,18,19 Bigliani and coworkers18 have determined that capsular injury is a significant factor in the development of anterior instability after finding that significant capsular stretching occurs before failure in their cadaveric model. Subsequently, Speer and associates2 reported on the results of a separate model, which demonstrated that Bankart lesions in isolation result in minimal anterior glenohumeral translations; they concluded that isolated Bankart lesions are not likely to be responsible for recurrent anterior shoulder instability. A cadaveric study of 16 scapulae by Itoi and colleagues22 in 2000 was used to investigate 10 separate fresh-frozen specimens in a custom multiaxial testing apparatus to determine that an osseous defect with a width at least
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instability in an attempt to elucidate which patients would benefit from conservative treatment or early aggressive surgical stabilization.
HH
Glenoid
Hill-Sachs lesion
Figure 21-3. Hill-Sachs lesion in a right shoulder. This is viewed from the posterior portal. HH, humeral head.
21% of the glenoid length (average width, 6.8 mm) may result in significant persistent instability and loss of functional ROM after Bankart repair. In addition, the clinicians noted that isolated Bankart repair in the setting of a large osseous defect may result in a dramatic loss of external rotation because the capsuloligamentous reconstruction overtensions the capsule to a glenoid that has lost concavity.22 This loss of external rotation is not only significant for short- and mid-term functional loss, but has been shown in other studies to produce unacceptable long-term results of early-onset glenohumeral arthrosis.29-32 These concerns become even more relevant when considering the results of a case-control study that demonstrated that the risk of developing severe arthrosis of the shoulder is from 10 to 20 times higher for individuals who have had a shoulder dislocation.33
Causative Factors and Natural History The lack of osseous constraint, combined with the broad ROM and translation of the glenohumeral joint, make it particularly susceptible to dislocation and recurrent instability. Chapters 17 and 19 present a thorough review of anterior and multidirectional instability. Our focus in this section are the aspects of anterior instability relevant to the diagnosis and treatment of Bankart lesions. The most common mechanism by which a Bankart lesion is sustained is through anterior dislocation of the shoulder, with the arm abducted and externally rotated. The abnormal translation of the humeral head that occurs in the process of dislocation results in a capsulolabral avulsion of the anterior or anteroinferior capsulolabral complex. Several studies have examined the risk factors for recurrent
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A classic study of conservative treatment for primary anterior shoulder dislocation was presented by Hovelius and associates28 in 1983. In this 10-year prospective multicenter Swedish study, 245 patients (247 shoulders) were assigned to one of three treatment groups as follows: (1) postreduction immobilization with arm secured to torso for 3 to 4 weeks; (2) postreduction use of a sling, which was discontinued after the patient became comfortable; and (3) postreduction immobilization for various durations. At the 10-year follow-up evaluation, 52% of shoulders had no subsequent dislocation, and recurrent instability requiring operative stabilization developed in 23%. Of the shoulders that developed recurrent instability requiring operative stabilization, there was a distinct difference in the percentage of recurrent instability relative to patient age—34% of patients 12 to 22 years, 28% of patients 23 to 29 years, and 9% of patients 30 to 40 years. This finding, that patients who are younger than 20 to 30 years are at a significantly increased risk of recurrent instability, is consistent with other studies in the literature that have reported recurrence rates of 83% to 95% for patients younger than 20 years, particularly in those who participate in athletics.34-36 Of additional interest, however, was the finding that 22% of the shoulders that sustained at least two recurrences during the initial 2- to 5-year follow-up period “stabilized spontaneously” at 10 years without surgical intervention.28 This latter finding is debatable and has been contested in the literature.37 Spontaneous stabilization of instability in this study has been proposed to be potentially related to age-related capsular changes and decreased physical demands in patients with increasing age.37 It must also be noted that less than 50% of patients in the study by Hovelius and coworkers28 sustained dislocations caused by a sports activity. It may therefore be inferred that their substantial but lower rate of recurrent instability requiring operative stabilization underestimates the risks of recurrent instability in young athletes (younger than 30 years) as reported in other studies. The natural history of recurrent instability for the athlete’s shoulder is a critical concept in determining operative indications and has not been definitively established in the literature. Patient-specific factors such as age, activity level, participation in contact or overhead athletics, and associated pathology play a critical role in patient counseling for the treatment of Bankart lesions. Simonet and Cofield36 have reported a recurrence rate of 82% after primary acute glenohumeral dislocation in athletes younger than 30 years. In a study of Swedish hockey players, Hovelius38 has reported a 90% rate of recurrence in patients younger than 20 and 65% in patients 20 to 25 years of age. Henry and Genung39 have reported a 95% rate of recurrence in a series of 100 patients, predominantly athletes, with almost
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75% requiring surgical stabilization to continue participation in athletics. Taylor and Arciero19 have reported a 90% recurrence rate in young athletes participating in collision sports. In a prospective randomized study of nonoperative treatment versus arthroscopic stabilization in patients with acute, traumatic, first-time shoulder dislocations, with 36-month average follow-up, Bottoni and colleagues have40 reported a 75% rate of recurrent instability in the nonoperative treatment group (4 weeks immobilization followed by a rehabilitation program). This is in contrast to an 11.1% recurrence rate for the group who underwent arthroscopic Bankart repair. Buss and associates41 have examined the results of nonoperative management for in-season athletes with anterior shoulder instability; they reported that 87% were able to return to sports for completion of the season without further injuries attributable to shoulder instability, despite 37% of patients experiencing at least one additional episode of instability during the season. In critically appraising the results of this study, it should be noted that 53% of patients in this study underwent subsequent surgical stabilization. A recent prospective, randomized, clinical trial by Kirkley and coworkers42 have compared the effectiveness of immediate arthroscopic stabilization with immobilization and rehabilitation for the treatment of primary traumatic anterior shoulder dislocation, with an average 75-month follow-up. They reported differences in the rate of redislocation for the two groups as well as for functional evaluation using the Western Ontario shoulder instability index questionnaire. No statistically significant difference was noted using the American Shoulder and Elbow Surgeons or disabilities of the arm, shoulder, and hand questionnaire. Based on these results, it was concluded that “immediate arthroscopic stabilization is the treatment of choice in a subset of patients who are younger than 30 years and are higher level athletes, and the timing for their surgery is good or their sport is risky.”42 Therefore, although it may be concluded that it is reasonable to consider a trial of conservative management after primary anterior glenohumeral dislocation in an athlete younger than 30 years, study results would support a substantial concern for recurrent instability in this population.
(e.g., Hill-Sachs, bony Bankart, glenoid and coracoid fractures). Specific views have been used to improve the sensitivity of detecting certain lesions, including the Stryker’s notch view for a Hill-Sachs lesion and West Point axillary view for a Bankart lesion. Magnetic resonance imaging (MRI), with or without gadolinium contrast injection, has become the primary imaging modality used for the assessment of shoulder instability. The acute MRI appearance of Bankart lesions typically shows a hemorrhagic effusion and elevation of the capsulolabral complex from the glenoid (Fig. 21-4). Usually, the scapular periosteum is also injured. If the capsulolabral injury extends medially and inferiorly, the lesion is referred to as an ALPSA (anterior labroligamentous periosteal sleeve avulsion).43 Takubo and colleagues44 have recently compared nonarthrographic MRI in abduction and external rotation with arthroscopic examination of the inferior glenohumeral ligament in 51 shoulders with traumatic anterior instability. They reported a 94% sensitivity and a 82% specificity for this MRI technique in assessing the inferior glenohumeral ligament. Limitations of traditional neutral positioning of the shoulder for routine MRI include the orientation of the anterior band of the inferior glenohumeral ligament (AIGHL) in a near-vertical orientation to the axial images, which supports the contention of several studies regarding the usefulness of abduction and external rotation when positioning the arm of the patient with anterior instability.44-46 In patients with bony deficiency resulting from a bony Bankart lesion, glenoid rim fracture, or large Hill-Sachs lesion, computed tomography (CT) with three-dimensional reconstructions is often useful for delineating the degree of bone loss and providing additional information about articular surface orientation and version.47
DIAGNOSIS AND ASSESSMENT OF BANKART LESIONS After a thorough history and physical examination documenting the neurovascular status of the involved extremity, the initial plain radiographic evaluation consists of anteroposterior (AP), true AP, axillary, scapular Y, and acromial outlet views. Although plain film imaging is an important initial modality in the workup of an anterior shoulder dislocation, its role is primarily to rule out associated fractures and identify frank osseous deformities
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Figure 21-4. Bankart lesion. This axial T1-weighted magnetic resonance imaging scan is of a right shoulder.
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In addition to the thorough physical examination performed in the office at the time of initial patient assessment, the examination under anesthesia is an imperative component of the workup and provides critical information for intraoperative decision making. Particular attention is given to ROM and degree of translation—anterior, posterior, and inferior. The distinction among asymptomatic, adaptive laxity, and pathologic instability, particularly in the overhead athlete’s shoulder, is not always clear. Thus, meticulous attention to detail when correlating the patient’s history, physical examination, diagnostic imaging, and examination under anesthesia provides the surgeon with the best chance for successful reconstruction and obtaining the maximal functional outcome.
OPERATIVE INDICATIONS The determination of operative indications for anterior shoulder stabilization in the setting of a Bankart lesion is predicated on patient age, activity level, history of shoulder pain or instability in the past, and desired future activity level. It is not unreasonable to consider a nonoperative approach for acute traumatic primary anterior dislocations in patients older than 40 years who do not desire to participate in recreational activities and have no evidence of gross instability or disruption of the normal osseous restraints to glenohumeral instability. After a brief period of immobilization (3 to 4 weeks), a functional rehabilitation program may allow for return to activities of daily living without further instability. If a patient develops recurrent instability, surgical stabilization would be indicated. A 3-year prospective observational cohort study of 538 patients by Robinson and associates48 has suggested that early operative stabilization is justified for patients with severe disruption of the soft tissue envelope caused by a large rotator cuff tear, disruption of the osseous restraints from a glenoid rim fracture, or combined glenoid rim fracture and greater tuberosity fracture with evidence of gross instability. The primary focus of our discussion here is the young athlete who desires to continue participation in sports after an acute, primary, traumatic, anterior shoulder dislocation.
BOX 21-1.
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This population, as noted, has a definitively increased risk for recurrent instability and several studies have supported early surgical stabilization.40,42,49 There is a spectrum of instability, however, and accordingly indications range from relative to absolute. Typical indications for surgical stabilization are listed in Box 21-1. The controversial issues regarding surgical stabilization with an arthroscopic or open approach will be discussed in detail.
ARTHROSCOPIC TECHNIQUES Procedural Approaches Several factors require thorough consideration when critically appraising the literature regarding arthroscopic Bankart repair. The debate over open and arthroscopic Bankart repair has unfolded during a period of rapid development of arthroscopic techniques and instrumentation for the treatment of anterior shoulder instability. Simultaneously, as noted, our understanding of the relevant basic science and biomechanical issues involved in shoulder instability has enabled us to develop and perform arthroscopic procedures that can achieve improved restoration of the capsulolabral complex and approximation of the native anatomy. Several issues become clear in reviewing the literature regarding arthroscopic Bankart repair. Initial results for arthroscopic Bankart repair with staple capsulorrhaphy have produced not only higher failure rates than open surgery, but an increased risk of complications.50 Subsequent techniques have included transglenoid suture and bioabsorbable tacks for Bankart repair. The former technique yielded varying results (0% to 49% failure rate) and had several limitations, including an inability to address capsular laxity adequately, medialization of the capsulolabral complex, the need to tie sutures over the posterior soft tissues, and the risk of suprascapular nerve injury.51 The technique of bioabsorbable tack fixation has produced somewhat lower failure rates, ranging from 9% to 23%, and represents a significant technical advance in the field of arthroscopy for labral repair and the treatment of instability.11,40,52-54 Disadvantages of this technique include its limited ability
Operative Indications for Anterior Shoulder Instability with a Bankart Lesion
Acute, primary, traumatic anterior dislocation in a young patient (⬍30 years) who participates in high-demand or high-risk athletics or activities with a propensity for recurrent instability (e.g., competitive overhead and contact athletes, construction workers, climbers) Acute, primary, traumatic anterior dislocation with a concomitant large rotator cuff tear or osseous compromise of the normal osseous restraints to glenohumeral instability Post-traumatic recurrent instability (subluxation or dislocation) limiting activities of daily living Pain related to persistent luxation after an acute, primary, traumatic anterior dislocation treated with an adequate nonoperative management program
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to address capsuloligamentous laxity and reports of a polyglycolic acid–induced synovitis.23,55 In 1996, Guanche and associates56 reported a 33% incidence of recurrent instability after arthroscopic Bankart repair with transglenoid sutures or a bioabsorbable tack; it was concluded that open stabilization is the procedure of choice. In retrospect, the critical technical flaw in the arthroscopic approach used in this study can be identified as a failure to mobilize and reconstruct the capsuloligamentous complex. A 2004 meta-analysis of six studies by Freedman and coworkers has concluded that arthroscopic Bankart repair with transglenoid sutures or bioabsorbable tacks results in a higher rate of recurrent instability (20.3% vs 10.3%; P ⫽ .01) and dislocation (12.6% vs 3.4%; P ⫽ .01) compared with open surgical techniques.51 In reviewing these data, one might conclude that arthroscopic Bankart repair produces inferior results compared with a traditional open surgical approach. However, in more recent studies, which used contemporary approaches to arthroscopic Bankart repair, addressed capsuloligamentous laxity, and used suture anchors, significantly improved results were obtained.42,49 In a 2003 prospective study of 167 patients with recurrent anterior shoulder instability treated with arthroscopic anterior stabilization that used suture anchors and a concomitant capsular shift, Kim and colleagues49 have reported a 4% failure rate, with an average follow-up of 44 months. Therefore, it becomes clear that it is imperative to consider more recent studies, which have used significantly improved techniques, when debating the strengths and limitations of arthroscopic and open surgery for anterior shoulder instability. In addition, it is clear that further prospective comparisons of contemporary arthroscopic techniques and open surgical approaches are needed, with adequate sample sizes, validated outcomes measures, and longer term follow-ups.
Theoretical Benefits of an Arthroscopic Approach There are several theoretical benefits of using an arthroscopic approach for the treatment of Bankart lesions, including selective tissue tensioning in restoring the capsuloligamentous anatomy, preservation of subscapularis integrity, improved postoperative ROM, and decreased postoperative pain. Suture anchors allow for precise restoration of the labrum at the glenoid face and concomitant capsulorrhaphy or capsular plication to reconstruct the anterior band of the inferior glenohumeral ligament. Some have suggested that assessment of capsular laxity and subscapularis deficiency in complex cases is best performed through an open approach.11,57 Others have proposed that these situations represent the cases for which arthroscopic assessment and treatment may be best suited. The magnification with which direct examination of the capsular tissue and subscapularis quality can be examined through the arthroscope may provide a more precise
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evaluation of structural integrity. Surgeon experience and technical skill clearly define the approach that is best suited for an individual case. However, current evidence in the literature would not support a statement claiming that open approaches categorically provide superior assessment.54
OPEN TECHNIQUES Open surgical treatment of Bankart lesions has been hailed in the literature as the gold standard. This approach has consistently provided reliable reproducible results, as reported in several studies.3,5,20,47
Anatomic Repairs The primary focus of our review will be on anatomic repairs, which are the most commonly performed procedures in North America. Nonanatomic repairs such as the Bristow, Latarjet, Magnuson-Stack, and Putti-Platt procedures are used with greater frequency in Europe—and occasional revision situations—and can yield low failure rates with regard to recurrent instability. Failure to address a Bankart lesion adequately with repair has been reported to be a major cause of failure when nonanatomic reconstructions are performed.58 In addition, the frequent complication of external rotation motion loss of up to 30 degrees has been associated with glenohumeral arthrosis.11,47 The Putti-Platt procedure was first described in 1948 by Osmond-Clarke. Familiarity with these procedures and their limitations and complications strengthens a shoulder surgeon’s ability to address complex revision situations with sound intraoperative decision making in cases for which capsular necrosis, poor soft tissue quality, and prior surgery limit options for reconstruction. In North America, the current standard for open Bankart repair and anterior shoulder stabilization is an anatomic repair that seeks to restore normal glenohumeral stability within the broadest arc of motion possible. This can be accomplished by addressing all pertinent labral and capsuloligamentous pathology without overconstraining the joint. Typically performed through a modified deltopectoral approach, which more closely parallels the anterior axillary fold, the subscapularis is divided with a vertical incision according to surgeon preference to provide maximal exposure of the glenohumeral joint and capsule, with minimal excess dissection and soft tissue trauma. Some have proposed a subscapularis-splitting horizontal approach to minimize the risk of postoperative rupture.59,60 The subscapularis is then meticulously dissected free from the anterior capsule and a capsulotomy is made medially, laterally, or in a T configuration for exposure of the glenohumeral joint. For open Bankart repair and anterior stabilization, we prefer the T-plasty modification of the Bankart procedure, as described in a 1991 study.5 With this technique, a vertical medial capsulotomy is made with a horizontal extension of the
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incision in a T configuration; this allows for tensioning of the superior and inferior flaps at the completion of the case before repair of the subscapularis. Bankart repair is most commonly performed through reattachment of the capsulolabral complex to the anterior glenoid rim with suture anchors. Suture anchors are lowprofile devices capable of providing stable fixation, with minimal articular surface compromise.61 With the use of suture anchors, the surgeon can specifically select the amount of tissue to incorporate at each level of the capsulolabral reconstruction and tension it accordingly by tying arthroscopic knots on the extra-articular side of the labrum. This technique allows not only for restoration of the labral bumper as a restraint to humeral head translation, but for restoration of the capsuloligamentous complex at an appropriate tension to restrain pathologic glenohumeral motion without excessive constraint.
Recommended Technique Our preferred technique is a follows. After induction of anesthesia, the patient is placed in the beach chair position on a beanbag with careful attention to padding all bony prominences and maintenance of a neutral cervical spine position. The beanbag is translated with the patient to the edge of the table and the entire scapula is exposed, with a medial bean buttress to stabilize it. A preoperative examination under anesthesia is performed to assess ROM and anterior, posterior and inferior translation, which are graded and documented. The patient is then prepared and draped in the usual sterile fashion and a marking pen is used to identify pertinent surface anatomic landmarks; these include the scapular spine, acromion, clavicle, and coracoid process. Arthroscopy is initiated from a standard posterolateral portal. For the performance of a Bankart repair and anterior stabilization, a far-lateral rotator interval portal is established just lateral to the biceps tendon and anterior to the leading edge of the supraspinatus. A second rotator interval portal is established more medially and inferiorly, just above the superior aspect of the subscapularis tendon. Cannula choice is predicated on patient size and anticipated repair location. We prefer to use a partially threaded 7-mm (inner diameter) cannula (Arthrex, Naples, Fla) for the more medial and inferior portal and a smaller Wolf cannula (ConMed Linvatec, Largo, Fla) for the accessory anterolateral portal. A curved spectrum instrument preloaded with polydioxanone suture (PDS) is shuttled through the anterior band of the inferior glenohumeral ligament and the capsulolabral complex inferiorly to shift this tissue superiorly and back up to the face of the glenoid (Fig. 21-5). After placement of the PDS, a pilot hole for a 3.0-mm BioSutureTak (Arthrex) is drilled at the peripheral margin of the glenoid face and the anchor is tapped into place. For revision situations and patients whose bone stock provides a suboptimal anchor purchase, a 3.7-mm BioSutureTak is available. This anchor is preloaded with a single no. 2 FiberWire (Arthrex) suture
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and is also available as a double-loaded anchor. The PDS is then securely attached to the extra-articular limb of the FiberWire suture and shuttled through the soft tissue. The extra-articular limb of the FiberWire suture then serves as the post for an arthroscopic knot to be tied under direct arthroscopic visualization to confirm optimal tensioning of the capsulolabral complex. This last step may be facilitated by switching the arthroscope from the posterior portal to the superolateral accessory portal, which provides a more direct view of the knot being tied through the more medial and inferior rotator interval portal. This process is performed at two or three points along the anterior inferior aspect of the glenoid sequentially, from inferior to superior. The portals are then closed in standard fashion and the extremity is placed in a sling.
REHABILITATION PRINCIPLES Selection of parameters for the postoperative rehabilitation protocol is critical to achieve a successful outcome after open or arthroscopic Bankart repair and anterior stabilization. We typically follow a six-phase program, as follows. Phase I. This consists of the first 3 weeks after surgery, during which the patient is immobilized in a sling with gradual incorporation of pendulum exercises and wrist and elbow ROM exercises. During this phase, active-assisted supine forward elevation to 90 degrees is allowed in addition to passive external rotation to neutral and shoulder abduction to 30 degrees. Scapula-tightening exercises and modalities are incorporated through participation in physical therapy. Phase II. This occurs during weeks 4 to 6 after surgery and begins with gradual discontinuation of the sling. Pulley exercises are then incorporated to encourage the development of full forward elevation, and active-assisted external rotation exercises are allowed to increase ROM from 0 to 30 degrees. Therapist-assisted, side-lying manual scapular stabilization exercises are initiated and pain-free internal and external rotation isometric exercises are performed in a neutral position. Phase III. This takes place during weeks 6 to 8 after surgery and involves the incorporation of biceps and triceps strengthening, progressive scapular strengthening within a protective arc (emphasizing closed-chain activities), and a further emphasis on increasing forward elevation and external rotation through active-assisted ROM exercises. Latissimus strengthening and the use of an upper body ergometer are initiated below 90 degrees of elevation and patients begin humeral head stabilization exercises when strength and ROM permit. Phase IV. This takes place during weeks 8 to 10 and focuses on aggressive periscapular muscle strengthening, as well as
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G
CLC
G
AID
CLC
HH HH 0
4
A
B
G
CLC
HH
C
8
D Figure 21-5. Bankart repair and anterior stabilization. A, Spectrum suture passer placing a polydioxanone suture (PDS) through the capsular tissue and underneath the anteroinferior labrum. B, Anchor insertion for Bankart repair. C, Suture shuttling (monofilament suture, PDS; braided suture, FiberWire (Arthrex, Naples, Fla). D, Bankart repair completed, with anatomic restoration of the capsulolabral complex. AID, anchor insertion device; CLC, capsulolabral complex; G, glenoid; HH, humeral head.
on deltoid, biceps, triceps, and latissimus strengthening as tolerated. Humeral head stabilization exercises receive a greater emphasis and proprioceptive neuromuscular facilitation pattern exercises are initiated. When patients are pain-free and have regained adequate strength, internal and external rotation exercises are incorporated with the arm in an elevated position. Phases V and VI. These final phases take place during weeks 10 to 24 after surgery. They focus more on upper extremity strengthening with eccentric exercises,
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development of coordinated scapulohumeral mechanics, endurance training, and sport-specific interval program.
COMPLICATIONS The primary complications of Bankart repair may be subdivided into perioperative and postoperative. Perioperative complications consist primarily of anchor failure, suture failure, glenoid rim fracture, musculocutaneous and axillary nerve injury, hematoma formation, and infection.
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Meticulous attention to detail during anchor placement (e.g., pilot hole placement and eyelet orientation) and to suture management will reduce the incidence of these complications. Glenoid rim fracture has been associated with the establishment of transosseous tunnels for Bankart repair; this has become less prevalent because the use of suture anchors has largely replaced this technique. Iatrogenic nerve injury may be avoided through a detailed knowledge of the regional anatomy and careful attention to retractor placement and arm positioning during open surgery.
surgeon considers the patient’s history, clinical examination, diagnostic imaging studies, future goals for functional outcome, and procedure that he or she thinks will most predictably and reliably yield an optimal outcome. Further prospective analysis of arthroscopic treatment of Bankart lesions in randomized controlled studies is needed to compare its success with that of open procedures and to identify the limitations of current techniques so that they may be improved.
Postoperative complications include recurrence of instability, subscapularis rupture (with open surgery), loss of motion (most commonly external rotation), implant failure and migration, premature arthrosis, and infection. As noted, a wide variation in recurrence rates has been reported in the literature for open and arthroscopic repairs. Pertinent issues to consider in evaluating the literature for recurrence rates include the criteria used by the authors (e.g., subluxation or dislocation and single or multiple episodes).42 Causes of recurrence have been described in detail earlier; these primarily include articular-arc compromise (bony Bankart and large, engaging Hill-Sachs lesions) and failure to address capsuloligamentous compromise.2,11,18,19,23 Subscapularis rupture has been described as a complication of open surgical reconstruction.62 Prompt recognition of this complication is critical to minimize the chance of a poor outcome and, as described by Neviaser and coworkers,63 should be suspected in all patients with recurrent instability and older patients after an anterior shoulder dislocation.47 Loss of external rotation may occur after Bankart repair and anterior stabilization,64 with the short-term consequence of failure to return to the desired preinjury level of activity and the long-term potential consequence of glenohumeral arthrosis caused by overconstraint of the glenohumeral joint.47 With careful attention to arm position during the performance of a selective capsular shift (open or arthroscopic), several studies have reported good results, with minimal loss of external rotation.49,65
1. Bankart ASB: The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 26:23-29, 1938. 2. Speer KP, Deng X, Borrero S, et al: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76: 1819-1826,1994. 3. Rowe CR, Patel D, Southmayd WW: The Bankart procedure. A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 4. Neer CS 2nd: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980. 5. Altchek DW, Warren RF, Skyhar MJ, et al: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone Joint Surg Am73:105-112, 1991. 6. Bigliani LU, Kurzweil PR, Schwartzbach CC, et al: Inferior capsular shift procedure for anteroinferior shoulder instability in athletes. Am J Sports Med 22:578-584, 1994. 7. Warner JJP, Johnson D, Miller M, et al: Technique for selecting capsular tightness in repair of anterior-inferior shoulder instability. J Shoulder Elbow Surg 4:352-364, 1995. 8. Wirth MA, Blatter G, Rockwood CA Jr. The capsular imbrication procedure for recurrent anterior instability of the shoulder. J Bone Joint Surg Am78:246-259, 1996. 9. Howell SM, Galinat BJ: The glenoid-labral socket: A constrained articular surface. Clin Orthop 243:122-125, 1989. 10. Iannotti JP, Gabriel JP, Schneck SL, et al: The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am 74:491-500, 1992. 11. Gill TJ, Zarins B: Open repairs for the treatment of anterior shoulder instability. Am J Sports Med 31:142-153, 2003. 12. Cooper DE, Arnoczky SP, O’Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum. J Bone Joint Surg Am 74:46-52, 1992. 13. Lazarus MD, Harryman DT II: Complications of open anterior stabilization of the shoulder. J Am Acad Orthop Surg 8:122-132, 2000. 14. Fehringer EV, Schmidt GR, Boorman RS, et al: The anteroinferior labrum helps center the humeral head on the glenoid. J Shoulder Elbow Surg 12:53-58, 2003. 15. Warner JJP, Caborn DNM, Berger R, et al: Dynamic capsuloligamentous anatomy of the glenohumeral joint. J Shoulder Elbow Surg 2:115-133, 1993. 16. Turkel SJ, Panio MW, Marshall JL, et al: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 17. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990.
CONCLUSION The debate continues in regard to the optimal treatment of Bankart lesions and anterior instability. The excellent results obtained with open surgical reconstruction in the past are now being reported with state-of-the-art arthroscopic approaches. It is critical to consider what techniques are being used when critically appraising the literature. Although open treatment was once the gold standard, we hesitate to use this term, because it implies that other procedures are suboptimal. Its use is therefore inappropriate when considering the dramatic technical advances in arthroscopic anterior stabilization that have been reported in recent studies. In the final analysis, the decision for which surgical approach to use is best made when the treating
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18. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 19. Taylor DC, Arciero RA: Pathologic changes associated with shoulder dislocations: Arthroscopic and physical examination findings in first time anterior dislocations. Am J Sports Med 25:306-311, 1997. 20. Gill TJ, Micheli LJ, Gebhard F, et al: Bankart repair for anterior instability of the shoulder. Long-term outcome. J Bone Joint Surg Am 79:850-857, 1997. 21. Mosely HF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913, 1962. 22. Itoi E, Lee SB, Berglund LJ, et al: The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: A cadaveric study. J Bone Joint Surg Am 82:35-46, 2000. 23. Burkhart SS, DeBeer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677-694, 2000. 24. Bigliani LU, Newton PM, Steinmann SP, et al: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med 26:41-45, 1998. 25. Saito H, Itoi E, Sugaya H, et al: Location of the glenoid defect in shoulders with recurrent anterior dislocation. Am J Sports Med 33:889-893, 2005. 26. Montgomery WH, Jr., Wahl M, Hettrich C, et al: Anteroinferior bone-grafting can restore stability in osseous glenoid defects. J Bone Joint Surg Am 87:1972-1977, 2005. 27. Hill HA, Sachs MD: The grooved defect of the humeral head. A frequently unrecognized complication of dislocations of the shoulder joint. Radiology 35:690-700, 1940. 28. Hovelius L, Eriksson K, Fredin H, et al: Recurrences after initial dislocation of the shoulder. Results of a prospective study of treatment. J Bone Joint Surg Am 65:343 -349, 1983. 29. Hawkins RJ, Angelo RL: Glenohumeral osteoarthrosis: A late complication of the Putti-Platt repair. J Bone Joint Surg Am 72:1193-1197, 1990. 30. Rosenberg BN, Richmond JC, Levine WN: Long-term followup of Bankart reconstruction: Incidence of late degenerative glenohumeral arthrosis. Am J Sports Med 23:538-544, 1995. 31. Matsen FA, Rockwood CA, Wirth MA, et al. Gleno-humeral arthritis and its management. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 870-872. 32. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment: Incidence and contributing factors. Am J Sports Med 32:1165-1172, 2004. 33. Marx RG, McCarty EC, Montemurno TD, et al: Development of arthrosis following dislocation of the shoulder: A casecontrol study. J Shoulder Elbow Surg 11:1-5, 2002. 34. Rowe CR: Prognosis in dislocations of the shoulder. J Bone and Joint Surg Am 38:957-977, 1956. 35. McLaughlin HL, MacLellan DI: Recurrent anterior dislocation of the shoulder: A comparative study. J Trauma 7:191-201, 1967. 36. Simonet WT, Cofield RH: Prognosis in anterior shoulder dislocation. Am J Sports Med 12:19-24, 1984.
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37. Arciero RA, Taylor DC, Hovelius L, et al: Correspondence. J Bone Joint Surg Am 80:299-300, 1998. 38. Hovelius L: Shoulder dislocation in Swedish ice hockey players. Am J Sports Med 6:373-377, 1978. 39. Henry JH, Genung JA: Natural history of glenohumeral dislocation-revisited. Am J Sports Med 10:135-137, 1982. 40. Bottoni CR, Wilckens JH, DeBerardino TM, et al: A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med 30:576-580, 2002. 41. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32:1430-1433, 2004. 42. Kirkley A, Werstine R, Ratjek A, et al: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 21:55-63, 2005. 43. Neviaser TJ: The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior instability of the shoulder. Arthroscopy 9:17-21, 1993. 44. Takubo Y, Horii M, Kurokawa M, et al: Magnetic resonance imaging evaluation of the inferior glenohumeral ligament: Non-arthrographic imaging in abduction and external rotation. J Shoulder Elbow Surg 14:511-515, 2005. 45. Neumann CH, Tirman PFJ, Steinbach LS, et al: Normal anatomy. In Steinbach LS, Tirman PFJ, Peterty CG, et al (eds): Shoulder Magnetic Resonance Imaging. Philadelphia, Lippincott-Raven, 1998, pp 1-36. 46. Kwak SM, Brown RR, Trudell D, et al: Glenohumeral joint: Comparison of shoulder positions at MR arthrography. Radiology 208:375-380, 1998. 47. Millett PJ, Clavert P, Warner JJP: Open operative treatment for anterior shoulder instability: When and why? J Bone Joint Surg Am 87:419-32, 2005. 48. Robinson CM, Kelly M, Wakefield AE: Redislocation of the shoulder during the first six weeks after a primary anterior dislocation: Risk factors and results of treatment. J Bone Joint Surg Am 84:1552-1559, 2002. 49. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 50. Coughlin L, Rubinovich M, Johansson J, et al: Arthroscopic staple capsulorrhaphy for anterior shoulder instability. Am J Sports Med 20:253-256, 1992. 51. Freedman KB, Smith AP, Romeo AA, et al: Open Bankart repair versus arthroscopic repair with transglenoid sutures or bioabsorbable tacks for recurrent anterior instability of the shoulder: A meta-analysis. Am J Sports Med 32: 1520-1527, 2004. 52. Laurencin CT, Stephens S, Warren RF, et al: Arthroscopic Bankart repair using a degradable tack. Clin Orthop 332:132-137, 1996. 53. Dora C, Gerber C: Shoulder function after arthroscopic anterior stabilization of the glenohumeral joint using an absorbable tack. J Shoulder Elbow Surg 9: 294-298, 2000. 54. Karlsson J, Magnusson L, Ejerhed L, et al: Comparison of open and arthroscopic stabilization for recurrent shoulder dislocation in patients with a Bankart lesion. Am J Sports Med 29:538-542, 2001.
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55. Edwards DJ, Hoy G, Saies AD, et al: Adverse reaction to an absorbable shoulder fixation device. J Shoulder Elbow Surg 3:230-233, 1994. 56. Guanche CA, Quick DC, Sodergren KM, et al: Arthroscopic versus open reconstruction of the shoulder in patients with isolated Bankart lesions. Am J Sports Med 24:144-148, 1996. 57. Geiger DF, Hurley JA, Tovey JA, et al: Results of arthroscopic versus open Bankart suture repair. Clin Orthop 337:1 11-117, 1997. 58. Rowe C, Zarins B, Ciullo J: Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am 66:159-168, 1984. 59. Jobe FW, Giangarra CE, Kvitne RS, et al: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 60. Andrews JR, Satterwhite YE: Anatomic capsular shift. J Orthop Tech 1:151-160, 1993.
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61. Rudzki JR, Purcell DB, Wright RW: Options for glenoid labral suture anchor fixation. Oper Tech Sports Med 12: 225-231, 2004. 62. Lazarus MD, Sidles JA, Harryman DT, et al: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability: A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 63. Neviaser RJ, Neviaser TJ, Neviaser JS: Concurrent rupture of the rotator cuff and anterior dislocation of the shoulder in the older patient. J Bone Joint Surg Am 70:1308-1311, 1988. 64. Lusardi DA, Wirth MA, Wurtz D, et al: Loss of external rotation following anterior capsulorraphy of the shoulder. J Bone Joint Surg Am 75:1185-1192, 1993. 65. Cohen SB, Altchek DW, Warren RF: Selective capsular shift approach for treatment of anterior and multidirectional shoulder instability. Tech Shoulder Elbow Surgery 2: 225-233, 2001.
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CHAPTER 22 Superior Labral Anterior-Posterior
Lesions of the Shoulder David A. Cortese and Stephen J. Snyder
Since the advent of arthroscopic techniques of evaluating and treating shoulder injuries in the 1980s, much has been learned about the insertion of the long head of the biceps tendon. The 20-power magnification provided by the arthroscope has led to the identification of lesions previously undetected by open surgical techniques. Over the ensuing years, various arthroscopic techniques have been developed to treat these lesions. Surgeons treating patients with shoulder injuries must have a good understanding of the normal anatomy, normal anatomic variants, and pathologic findings associated with this region, and must be adept in the arthroscopic skills developed to treat these lesions.
Typically, the inner edge of the labrum is firmly attached to and continuous with the hyaline cartilage of the glenoid surface. Superiorly, the labrum may occasionally have a more meniscal appearance, with the inner edge attached only loosely to the glenoid, a variation seen in approximately 15% of patients (Fig. 22-1). The anterosuperior labrum is the area from the anterior insertion of the biceps tendon to the anterior midglenoid notch, and is the area where anatomic variants are most common. In the usual situation (in approximately 80% of patients), the anterosuperior labrum is firmly and smoothly attached to the glenoid articular cartilage. The middle glenohumeral ligament appears as a thickening of the anterior capsule that crosses over the subscapularis tendon at an angle of about 45 degrees and inserts onto the anterosuperior glenoid neck just medial to the labrum (Fig. 22-2).
BACKGROUND The first description of labral tears involving the superior aspect of the glenoid labrum was made in 1984 by Andrews and colleagues1 in a report on 73 overhead athletes. They hypothesized that the lesion is a traction injury caused by the biceps tendon pulling off the labrum. In 1990, Snyder and associates2 reported on 27 patients with a specific injury pattern involving the superior aspect of the labrum identified as part of a retrospective review of 700 shoulder arthroscopies. They found that the lesion extends anteriorly and posteriorly from the insertion of the biceps tendon, and coined the term SLAP (superior labral anterior-posterior) lesion. Although not common and difficult to diagnose clinically, SLAP lesions can be a significant cause of disability, particularly in the overhead athlete.
It is important to recognize two normal variants for anterosuperior labral anatomy to diagnose labral abnormalities accurately. One variant involves an opening beneath the labral attachment of the anterosuperior labrum, termed a sublabral foramen. This foramen may be as small as 1 or 2 mm or extend along the entire anterosuperior quadrant (Fig. 22-3). As long as the opening is superior to the midglenoid notch and inferior to the anterior insertion of the biceps tendon, it is likely a normal variant. The second situation is the so-called Buford complex.3 This anatomic variant, described in 1994, consists of a cordlike middle glenohumeral ligament that attaches directly to the superior labrum at the anterior insertion of the biceps tendon. The anterosuperior labrum is completely absent and the thickened, cordlike, middle glenohumeral ligament crosses over the subscapularis tendon (Fig. 22-4). The anteroinferior labrum has a normal appearance below the mid glenoid notch. This anatomic variant is often incorrectly identified as a labral tear. If the thickened ligament is attached to the glenoid in an attempted repair, it will severely limit external rotation.
ANATOMY The glenoid labrum is a fibrocartilaginous structure that surrounds the glenoid and aids in shoulder stability by deepening the concavity of the glenoid. The vascular supply to the labrum arises from branches of the suprascapular, circumflex scapular, and posterior circumflex humeral arteries. Similar to the menisci of the knee, the labrum receives its blood supply from capsular and periosteal vessels through the periphery rather than the underlying bone, and the inner edge is relatively avascular.
CLASSIFICATION The original classification of SLAP lesions was proposed in Snyder’s 1990 article2 and consists of four types:
The supraglenoid tubercle is approximately 5 mm medial to the articular surface of the glenoid at the 12-o’clock position. The long head of the biceps tendon originates from the superior labrum and the supraglenoid tubercle.
Type I lesions involve degenerative fraying of the free edge of the superior labrum, similar to a degenerative meniscus in 269
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Sublabral hole
A Figure 22-1. Arthroscopic image showing normal variant of superior labrum with meniscoid appearance.
the knee; however, the attachment of the peripheral labrum and biceps tendon to the glenoid remains intact (Fig. 22-5). These lesions were found to comprise 21% of cases in a study of 140 SLAP lesions.4 Type I SLAP lesions are usually found in middle-aged and older patients and are not considered to be a common source of clinical symptoms. Type II SLAP lesions are the most common, occurring in 55% of patients in the same study.4 This lesion may be
B Figure 22-3. Arthroscopic image (A) and diagrammatic representation (B) of a sublabral foramen (arrow), a normal anatomic variant.
associated with variable fraying of the edge of the labrum, as in type I lesions; however, it also involves significant detachment of the superior labrum and biceps anchor from the superior glenoid (Fig. 22-6). Traction on the biceps tendon causes the biceps anchor–superior labral complex to arch away from the glenoid neck. Depending on the extent of the detachment, a type II SLAP lesion may undermine the labral insertions of the superior and middle glenohumeral ligaments and result in some degree of anterior instability.
Figure 22-2. Arthroscopic image showing normal appearance of anterosuperior quadrant.
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Type III SLAP lesions are less common, occurring in only 9% of patients. This lesion involves a split of a meniscoid superior labrum, forming a mobile, bucket-handle labral fragment (Fig. 22-7). The biceps tendon and peripheral labral attachment to the superior glenoid are intact. Symptoms develop as a result of catching of the mobile labral
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(1) Biceps tendon (2) Cordlike MGHL
(3) Absent anterior-superior labrum
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Figure 22-4. Arthroscopic image (A) and diagrammatic representation (B) of a Buford complex, a normal anatomic variant.
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Figure 22-5. Diagrammatic representation (A) and arthroscopic image (B) of a type I superior labral anterior-posterior (SLAP) lesion.
fragment within the joint. Occasionally, the middle glenohumeral ligament may be attached to the torn fragment and thus be rendered unstable.
involve bucket-handle tears of the labrum associated with an unstable labrum and anchor, and are thus classified as complex SLAP types II and III or types II and IV lesions.
Type IV SLAP lesions are also relatively uncommon, seen in only 10% of patients. Like the type III SLAP lesion, this lesion involves a bucket-handle tear of a meniscoid superior labrum but, in this case, the tear extends into the biceps tendon (Fig. 22-8). The biceps tendon fragment may displace into the joint with the labral fragment, causing clinical symptoms.
Since Snyder’s original description, others have expanded the classification. Morgan and coworkers5 have subclassified type II SLAP lesions into anterior, posterior, and combined anterior-posterior lesions. Maffet and colleagues6 have described three additional types: (1) anteroinferior labral separation extending superiorly to undermine the biceps anchor; (2) biceps tendon separation with an unstable flap tear of the labrum; and (3) extension of the superior labrum–biceps tendon separation anteriorly to undermine the middle glenohumeral ligament.
Complex SLAP lesions, which are combinations of the four basic types, have also been observed. Most commonly, these
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Figure 22-6. Diagrammatic representation (A) and arthroscopic image (B) of a type II superior labral anterior-posterior (SLAP) lesion.
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Figure 22-7. Diagrammatic representation (A) and arthroscopic image (B) of a type III superior labral anteriorposterior (SLAP) lesion.
DIAGNOSIS The clinical diagnosis of a SLAP lesion is difficult and requires a high index of suspicion on the part of the treating physician. This is in part a result of the association of SLAP lesions with other shoulder maladies. In a study of 140 patients with injuries to the superior labrum, Snyder and associates4 found that only 28% of the SLAP lesions are isolated injuries. Conditions associated with SLAP lesions include partial and complete rotator cuff tears, Bankart lesions, impingement, acromioclavicular arthrosis, and supraglenoid ganglion cysts.
trauma, such as a fall or motor vehicle accident, or of chronic overuse, such as throwing or striking a ball. Patients may complain of a vague pain or discomfort that limits athletic performance and is located deep in the joint or in the posterior aspect of the shoulder. The pain is usually aggravated by overhead activity, particularly with the cocking phase of throwing. Mechanical symptoms of catching or popping are also common. Complaints of night pain, weakness, or instability are not uncommon and may be caused by associated pathology, as described earlier.
SLAP lesions typically occur in young and active male patients. The onset of symptoms may be the result of acute
In the acute injury, the mechanism is believed to be a compressive force between the humeral head and glenoid. The
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Figure 22-8. Diagrammatic representation (A) and arthroscopic image (B) of a type IV superior labral anterior-posterior (SLAP) lesion.
cause is often a fall onto a slightly abducted and flexed shoulder, which drives the head superiorly against the labrum and biceps anchor and results in increased tension in the biceps tendon as it courses over the humeral head. In the chronic overuse injury, the patient reports insidiously progressive symptoms that limit performance in overhead sports. Burkhart and coworkers have proposed a peel-back mechanism, in which abduction and external rotation cause a twisting at the base of the biceps tendon and result in a tear that begins anteriorly and extends posteriorly with time. In addition to the history, a thorough physical examination is essential for making a clinical diagnosis. However, because of the presence of associated pathology, the physical examination may be nonspecific or confusing. Various specific tests have been described to help in the clinical diagnosis of a SLAP lesion. Biceps tension tests, such as the Speed’s test and O’Brien’s test, are typically positive in patients with type II lesions because of the instability of the biceps anchor. Speed’s test is performed by positioning the patient’s arm in 90 degrees of forward flexion at the shoulder, with the elbow extended and the forearm supinated, while the patient resists a downward force applied to the patient’s wrist. O’Brien’s test is similar, with the arm positioned in 90 degrees forward flexion and 20 degrees adduction at the shoulder (Fig. 22-9). A downward force applied at the wrist is resisted with the forearm in a supinated and then a pronated position, comparing the two results. A positive test result is when the pain is worse in the pronated position. Other useful tests involve a compressive load applied to the labrum that elicits pain or mechanical symptoms. The compression rotation test is similar to the McMurray test for meniscal pathology in the knee. This test is
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performed by positioning the patient’s arm with the shoulder abducted 90 degrees, applying a compressive load, and internally and externally rotating the humerus on the glenoid (Fig. 22-10). The crank test, as described by Liu and colleagues8 in 1996 is similar, except that the arm is in extreme elevation (to 160 degrees) in the scapular plane while the shoulder is compressed and rotated. The anterior slide test was described by Kibler in 1995.9 The patient positions his or her arm with the hand on the hip, with the thumb facing posteriorly. The examiner stabilizes the scapula with one hand while the patient resists a superiorly and anteriorly directed force applied to the glenoid through the elbow and upper arm. The ability of these tests to predict SLAP lesions conclusively and reliably has been debated. In each study describing a new diagnostic test, the sensitivity and specificity of the test are reportedly high, typically 90% or higher. However, these results have not been obtained in studies by other clinicians, including ourselves. Several studies comparing the clinical value of various tests have
Figure 22-9. O’Brien’s test performed with shoulder flexed 90 degrees and adducted 20 degrees, elbow extended, and forearm pronated.
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Figure 22-10. Compression-rotation test.
Figure 22-11. Arthroscopic image of superior labral anterior-posterior (SLAP) fracture of the superior humeral head.
shown that no single test or combination of tests can conclusively or reliably predict a SLAP lesion.10-12 Radiographic imaging studies can aid in the diagnosis when the clinical examination is suggestive of labral injury. Conventional radiographs may reveal characteristic findings for associated shoulder anomalies, such as subacromial impingement, degenerative arthritis, and instability. Occasionally, a SLAP fracture may be seen on plain radiographs, but typically they are of little value in diagnosing SLAP lesions (Fig. 22-11). Ultrasound imaging has not proved useful in identifying labral injuries. Computed tomography (CT) arthrography has improved the detection of labral pathology, but it is better at defining abnormalities of bone than of soft tissue. Magnetic resonance imaging (MRI) has proved useful for evaluating soft tissue pathology about the shoulder, particularly for injuries of the rotator cuff, biceps tendon, and capsule. MRI has been shown to have good sensitivity and specificity for identifying injuries of the anterior and inferior labrum, and the presence of a supraglenoid cyst on an MRI scan is suggestive of a superior labral tear (Fig. 22-12). However, conventional MRI techniques are somewhat limited for evaluating injuries to the superior labrum. In an effort to increase the accuracy of MRI for evaluating labral injuries, MR arthrography using intra-articular injection of dilute gadolinium has gained widespread use. The SLAP lesion is best appreciated on coronal oblique images as a distinct cleft extending medially beneath the biceps anchor between the superior labrum and cortical surface of the glenoid. The contrast often diffuses into the labral fragment, causing it to have a ragged, indistinct appearance (Fig. 22-13). In a study
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Figure 22-12. Magnetic resonance imaging scan of a supraglenoid cyst (arrow) suggestive of a superior labral tear.
comparing results of MR arthrography with those of diagnostic arthroscopy, Waldt and associates13 have found that MR arthrography shows a sensitivity of 82% and specificity of 98% for the detection of SLAP lesions, but that the technique has limited ability in classifying the type of SLAP lesion.
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Figure 22-13. Magnetic resonance arthrogram of a superior labral anterior-posterior (SLAP) lesion.
Because of the limitations of the history, physical examination, and imaging studies to diagnose SLAP lesions definitively, a high index of suspicion should be maintained by the treating physician. In the young athletic male patient with persistent shoulder pain, whose symptoms and clinical findings are not consistent with those of other diagnostic entities, labral pathology should be considered. Ultimately, the diagnosis of SLAP lesions is often only made by performing an accurate diagnostic shoulder arthroscopy. A complete diagnostic arthroscopic examination should be performed, with particular attention paid to the anterosuperior quadrant. Findings consistent with SLAP lesions include hemorrhage or granulation tissue beneath the biceps anchor and superior labrum, the presence of a space between the peripheral articular cartilage margin of the glenoid and attachment of the labrum and biceps anchor, and displacement of the superior labrum and biceps anchor more than 3 or 4 mm away from the glenoid when traction is applied to the biceps tendon (Fig. 22-14).
TREATMENT Treatment of SLAP lesions is based on lesion type. Because type I SLAP lesions are degenerative and by definition do not involve instability of the labrum or biceps anchor, they are treated with débridement of the frayed labrum to address pain and mechanical symptoms. A 4.0-mm full-radius shaver is used to remove only the damaged labral tissue, being careful to preserve the anterosuperior labral attachment, biceps anchor, and insertion of the middle glenohumeral ligament.
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Figure 22-14. Arthroscopic image of a type II superior labral anterior-posterior (SLAP) lesion that displaces when traction is applied to the bicep tendon (arrow).
Type II SLAP lesions are repaired using a single-anchor, double-suture technique (see later,“Single-Anchor DoubleSuture SADS Repair for Type II SLAP Lesions”). A 4-mm Big Eye Revo anchor (ConMed Linvatec, Largo, Fla) or similar suture anchor is loaded with two strands of strong braided suture and inserted into the superior glenoid just below the biceps tendon. The sutures are placed through the labrum and one is then directed anteriorly and one posteriorly around the biceps, forming a sling around the anchor and providing secure fixation of the labrum for healing. Type III SLAP lesions are treated with resection of the bucket-handle labral fragment, followed by close inspection of the remaining labrum for stability. A basket punch is first used to divide the posterior attachment of the bucket handle and then a shaver is used to remove the labral fragment. Careful attention is made to ensure that the attachment of the middle glenohumeral ligament (MGHL) is not compromised before completing the resection. If a cordlike MGHL is attached to the anterior fragment of the torn labrum, a robust anterior tag is left to preserve the attachment. This tag should be reattached to the glenoid with a suture anchor if traction on the ligament reveals instability of the MGHL. Type IV lesions are treated based on the severity of biceps tendon involvement. In patients with minimal involvement of the tendon, the involved tendon is excised along with the labral fragment, as in type III lesions. If more than 30% of the tendon is involved with the displaced labral tear, repair of the tendon should be considered to release it and repair the labrum, as in type II lesions, or to tenodese the end of the tendon to bone. The treatment choice
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depends on the age and activity level of the patient and condition of the remaining portion of the tendon. In most cases, the labral fragment and involved portion of the biceps tendon are excised. If the remaining tendon appears degenerative and frayed, or the anchor site is unstable, the tendon should be released and often tenodesed, especially in the young active patient. When encountered, complex types II and III or complex types II and IV lesions can be treated using the principles described earlier. Torn segments of the labrum and biceps tendon can be débrided and, if the remaining portion of the biceps anchor is substantial and unstable, it can be repaired back to the glenoid using the technique described later for repair of type II SLAP lesions. Because SLAP lesions usually occur with concomitant shoulder abnormalities, it has been difficult to interpret results of suture anchor repair techniques. Stetson and colleagues14 have evaluated a subset of 23 patients with isolated SLAP lesions, with average follow-up of 3.8 years (range, 14 months to 8 years). Of the 23 SLAP lesions studied, 1 type I lesion was treated with débridement, 6 type II lesions were treated with débridement and abrasion, 12 type II lesions were treated with fixation using one of three suture anchors, 1 type III lesion was treated with débridement, 2 type IV lesions were treated with débridement, and 1 complex types II and III lesion was treated with a combination of débridement and fixation with an absorbable anchor. Based on the Rowe scoring system at final follow-up, 82% of patients had good or excellent results, 9% had fair results, and 9% had poor results. Of the two patients with poor results, one had a type II SLAP lesion that was treated with débridement alone and ultimately required open anterior shoulder stabilization. The other patient had a type IV SLAP lesion treated with
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débridement that was clinically unstable on follow-up. Of the two patients with fair results, one had a complex types II and III lesion that had cracking in the joint and ultimately required removal of the absorbable tack fragments. The second patient had a type III SLAP lesion that was treated with débridement. Notably, all three patients whose type II SLAP lesion was treated with a screw-type suture anchor were able to return to their previous level of sports competition. Kim and associates15 have also reported their results of 34 patients with isolated SLAP lesions who underwent arthroscopic repair with suture anchors, with a mean follow-up of 33 months. Based on the UCLA shoulder score at final follow-up, 32 patients (94%) had a satisfactory result, and 2 patients had an unsatisfactory result. Of 34 patients, 31 (91%) regained their preinjury level of shoulder function. However, they reported inferior results in overhead throwing athletes compared with patients not involved in overhead sports.
Single-Anchor Double-Suture SADS Repair for Type II SLAP Lesions The single-anchor double-suture (SADS) SLAP repair can be performed with the following steps: 1. Begin with the arthroscope in the standard posterior superior portal (PSP). Create an anterior superior portal (ASP) using an outside-in technique with a spinal needle. The proper placement of the portal is in the superior aspect of the rotator interval, anterior and slightly superior to the biceps tendon (Fig. 22-15). The needle is inserted at a point approximately 2 cm from the anterolateral corner of the acromion, and the path of the needle must approach the superior tubercle of the
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Figure 22-15. Diagrammatic representation (A) and arthroscopic image (B) illustrating creation of an anterior-superior portal using the outside-in technique with spinal needle.
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glenoid at an angle of 45 degrees, just posterior to the biceps tendon. Once the needle is properly positioned, the portal is created using a smoothwalled crystal cannula (Arthrex, Naples, Fla). 2. Create an anterior midglenoid portal (AMGP) using an outside-in technique by placing a spinal needle just superior to the subscapularis tendon at a position midway between the glenoid surface and tuberosity. A second smooth cannula is placed through this portal. 3. Débride the fibrous tissue down to cancellous bone from the superior glenoid below the detached labrum and biceps anchor using a 4-mm full-radius shaver (Fig. 22-16). It is often useful to débride the posterior aspect of the superior glenoid
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with the shaver in the PSP and arthroscope in the AGMP. Conversely, the anterior aspect of the superior glenoid is more easily débrided with the shaver in the AGMP and the arthroscope in the PSP. 4. Create a pilot hole for a suture anchor in the superior tubercle of the glenoid by placing a Revo punch through the cannula in the ASP, posteriorly around the biceps tendon. The tip of the punch should be directly below the biceps tendon, at the midpoint of the biceps anchor anteriorly and posteriorly, and 2 to 3 mm medial to the articular cartilage (Fig. 22-17). Carefully observe the insertion of the punch to ensure that it does not skive off the bone into the articular cartilage or down the neck of the glenoid. The handle of the punch
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Figure 22-16. Diagrammatic representation (A) and arthroscopic image (B) illustrating preparation of a superior glenoid by débridement of fibrous tissue with 4-mm shaver.
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Figure 22-17. Diagrammatic representation (A) and arthroscopic image (B) illustrating creation of a pilot hole for suture a anchor placement using an anchor punch with tip seated 3 mm medially to the articular surface of glenoid.
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should be maneuvered laterally and posteriorly to direct the tip into the bone (Fig. 22-18). Prepare a 4-mm Big Eye Revo or 5-mm SuperRevo anchor (ConMed Linvatec, Largo, Fla) by loading it with two no. 2 nonabsorbable, braided sutures. To facilitate suture management, one suture should be white and one green. One half of each suture is colored purple so that there are four differently colored suture limbs for easier suture management, with the purple-colored limbs exiting on the same side of the anchor eyelet (Fig. 22-19). Place the anchor through the cannula in the ASP, posterior to the biceps tendon and into the pilot hole. Seat the anchor to the appropriate depth and align it so that the purple-colored suture limbs are oriented toward the biceps tendon (Fig. 22-20). Test the anchor security by gently pulling on the sutures. Retrieve both the all-white and all-green suture limbs out through the cannula in the AMGP with a crochet hook (Fig. 22-21). Store the suture limbs outside the cannula by inserting a switching stick, removing the cannula, and then replacing the cannula with both suture limbs outside the cannula. Retrieve both the white-purple and green-purple sutures out through the cannula in the AMGP with a crochet hook (Fig. 22-22). These sutures will be passed through the labrum together to form the stitch of Burns. Insert a medium Spectrum Crescent hook loaded with a Shuttle Relay Suture Passer (both from ConMed Linvatec, Largo, Fla) through the cannula into the ASP. Pierce the biceps tendon at the midpoint of the biceps anchor, and angle the tip to exit just below the labrum and above the suture anchor. Insert a grasper through the cannula in the AMGP following the path of the whitepurple and green-purple suture limbs. Pass 3 cm
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Figure 22-18. Direction of insertion of anchor punch with handle pushed laterally and posteriorly (arrow).
Figure 22-19. Four-mm Revo anchor with suture ends prepared for insertion and simplifying suture management.
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Figure 22-20. Diagrammatic representation (A) and arthroscopic image (B) illustrating insertion of a suture anchor (A, inset) through an anterior-superior portal into pilot hole.
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Figure 22-21. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval of different-colored sutures out through the cannula in the anterior midglenoid portal.
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Figure 22-22. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval of different-colored sutures out through the anterior midglenoid portal.
of the Shuttle Relay Suture Passer into the joint, secure it with the grasper, and retrieve it into the cannula in the AMGP (Fig. 22-23). 9. Load the Shuttle Relay Suture Passer with both purple-colored suture limbs and draw them back through the labrum and out through the cannula in the ASP, being careful to ensure that they are not twisted around the other suture limbs (Fig. 22-24). 10. Retrieve the white-purple suture limb back into the AMGP. Retrieve the all-green suture limb into the cannula in the ASP using a crochet hook. This suture limb needs to be directed posterior to the biceps tendon (Fig. 22-25). Shorten the greenpurple suture limb to act as a post, and tie a sliding-locking knot to secure the posterior aspect of the superior labrum to the anchor (Fig. 22-26).
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11. Retrieve both the all-white and the white-purple suture limbs into the cannula in the ASP anterior to the biceps tendon using a crochet hook (Fig. 22-27). Shorten the white-purple limb to act as a post. Tie a sliding-locking knot to secure the anterior aspect of the superior labrum to the anchor. 12. Test the repair by pulling on the biceps tendon with a probe through the AMGP (Fig. 22-28). The labrum should be firmly secured and there should be no gap when tension is applied.
POSTOPERATIVE CARE Postoperatively, the operative extremity is placed into a 15-degree external rotation shoulder sling for 4 weeks. The patient is encouraged to perform gentle range-of-motion
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Figure 22-23. The Spectrum Crescent Hook is passed through the middle of the biceps anchor and the Shuttle Relay Suture Passer is retrieved through the anterior midglenoid portal.
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Figure 22-24. Diagrammatic representation (A) and arthroscopic image (B) illustrating passage of different-colored sutures through the biceps anchor and out through the anterior superior portal.
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Figure 22-25. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval (A, inset) of different-colored sutures out through the anterior superior portal.
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Figure 22-26. Diagrammatic representation (A) and arthroscopic image (B) illustrating a sliding knot being tied posterior to a biceps tendon to secure posterosuperior labrum to glenoid rim.
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Figure 22-27. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval (A, inset) of different-colored sutures out through the anterior superior portal.
(ROM) exercises of the elbow, wrist, and hand in the immediate postoperative period. Pendulum and passive ROM exercises begin 1 week after surgery. It is important to protect the shoulder from excessive stress on the biceps tendon for 6 weeks, so the patient is instructed to avoid any lifting with the operative extremity. Progressive resistance exercises begin at 6 weeks after surgery, with vigorous throwing and heavy lifting activities delayed until 3 months, provided that painless motion has returned to normal.
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SUMMARY A wide variety of pathology may affect the superior aspect of the labrum. Clinical examination is often difficult because of the numerous injury mechanisms and variable extent of labral pathology. Proper identification of the exact mechanism and specific severity of pathology is vital to diagnose and manage these injuries accurately. Surgical procedures to address SLAP lesions vary from minimal débridement to extensive labral repair. Postoperative
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Figure 22-28. Diagrammatic representation (A) and arthroscopic image (B) showing appearance of final repair with one knot tied anterior and one knot tied posterior to biceps tendon.
rehabilitation must be based on the specific injury and surgical procedure performed, as well as on an understanding of the basic science related to injury and tissue healing. References 1. Andrews JR, Carson WG, McLeod WD: The arthroscopic treatment of glenoid labrum tears—the throwing athlete. Orthop Trans 8:44, 1984. 2. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990. 3. Williams MM, Snyder SJ, Buford D Jr: The Buford complex— the “cord-like” middle glenohumeral ligament and absent anterosuperior labrum complex: A normal anatomic capsulolabral variant. Arthroscopy 10:241-247, 1994. 4. Snyder SJ, Banas MP, Karzel RP: An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg 4: 243-248, 1995. 5. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationship to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 6. Maffet MW, Gartsman GM, Mosley B: Superior labrumbiceps tendon complex lesion of the shoulder. Am J Sports Med 23:93-98, 1995. 7. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions
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and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 8. Liu SH, Henry MH, Nuccion SL: A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med 24:721-725, 1996. 9. Kibler WB: Specificity and sensitivity of the anterior slide test in throwing athletes with superior glenoid labral tears. Arthroscopy 11:296-300, 1995. 10. Guanche CA, Jones DC: Clinical testing for tears of the glenoid labrum. Arthroscopy 19:517-523, 2003. 11. Holtby R, Razmjou B: Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: Comparison with arthroscopic findings. Arthroscopy. 20:231-236, 2004. 12. McFarland EG, Kim TK, Savino RM: Clinical assessment of three common tests for superior labral anterior-posterior lesions. Am J Sports Med 30:810-815, 2002. 13. Waldt S, Burkart A, Lange P, et al: Diagnostic performance of MR arthrography in the assessment of superior labral anteroposterior lesions of the shoulder. AJR Am J Roentgenol 182:1271-1278, 2004. 14. Stetson WB, Snyder SJ, Karzel RP: Long-term clinical followup of isolated SLAP lesions of the shoulder. Presented at the 65th Annual Meeting of the American Academy of Orthopedic Surgeons, New Orleans, March 1998. 15. Kim SH, Ha KI, Kim SH, Choi HJ: Results of arthroscopic treatment of superior labral lesions. J Bone Joint Surg Am 84:981-985, 2002.
9/19/08 7:09:43 PM
CHAPTER 23 Soft Tissue Injuries
of the Shoulder Judson W. Ott, William G. Clancy, Jr., and Kevin E. Wilk
There are a multitude of painful soft tissue injuries about the shoulder. Most of these injuries are a result of primary injury to the tendon sheath or primary fatigue failure within the tendon. Additional injuries may result from complete or partial rupture of a tendon or the muscle tendon complex, whereas other painful conditions are caused by acute or chronic bursitis or bony impingement.
only the tendon sheath in those with acute tendinitis. Biopsies of patients with chronic tendinitis, as reported by Clancy5 and Nirschl,7,8 have indicated a complete absence of inflammatory cells in the tendinous tissue itself, particularly in areas of tendon degeneration; it was noted that inflammatory cells are found only in those patients with gross partial ruptures. This lack of inflammatory cells has been noted by Becker and Cofield9 on histologic examination of the biceps tendon. These areas are characteristic in that there is a loss of the normal collagen architecture and a paucity of tenocytes. Degenerative changes within a tendon in patients who were asymptomatic and histologic examination showed no signs of inflammation; this was described by Puddu and colleagues10 as representing a condition termed tendinosis. More appropriately, Clancy5 has used the term paratenonitis with tendinosis to describe more accurately the clinical and histologic findings in those patients with classic symptomatic tendinitis.
TENDINITIS, BURSITIS, AND THE INFLAMMATORY RESPONSE Most soft tissue injuries about the shoulder occur as a result of primary failure within a tendon, with pain emanating from the inflammatory repair response within the tendon sheath. Inflammation can be thought of as a series of steplike processes, beginning with vasal dilation mediated by histamine, serotonin, and kinins, followed by the appearance of gaps in the endothelial cells, resulting in increased vascular permeability and subsequent local tissue inflammation. Inflammatory cells, such as leukocytes, are drawn to a specified area by a process known as chemotaxis.1,2 Acute inflammation typically lasts hours to days. If the initiating stimuli continues, the inflammatory response will produce a thickened, chronically inflamed tendon sheath. The process of inflammation is perceived as pain through the detection of noxious stimuli by afferent nerve fibers.3 These consist primarily of two fiber types—the unmyelinated, slow-conducting C fibers, which are responsible for dull, aching, or burning-type pain, and the finely myelinated, fast-conducting A gamma fibers, which are important in the perception of joint pain.3 These nerve endings become sensitized to the release of tissue mediators and prostaglandins; inflammatory mediators may moderate the release of neural peptides, all of which are ultimately perceived through peripheral nerves, transported to the central nervous system, and perceived as pain.
Bursitis is an inflammation of the synovial sac, which is generally present at any site at which increased friction may develop. The olecranon, greater trochanter, and patella are three of the common areas in which bursal inflammation may occur. A bursa is located between the superomedial angle of the scapula and the underlying rib cage and may become inflamed as a result of mechanical irritation. Even though bursal tissue is usually located in areas of friction, a bursa may also act as a tendon sheath in some locations. The subacromial and subdeltoid bursa represents the tendon sheath of the rotator cuff and, as such, may be primarily inflamed because of mechanical irritation by the coracoacromial ligament or by anterolateral impingement of the acromion. It may be secondarily inflamed when there is failure within the tendon, manifested as a partial or complete rupture of any of the cuff tendons. It is almost impossible to differentiate clinically rotator cuff bursitis as primary or secondary unless there is adequate biopsy material from the rotator cuff tendon. We think that in the young throwing athlete, the primary entity is a bursitis caused by mechanical impingement from the coracoacromial ligament, without rotator cuff pathology.
Tendinitis, as described by Clancy4,5 and Clement and colleagues,6 is believed to represent devitalization and disruption of tendon fascicles caused by repetitive microtrauma. Some unknown mechanism stimulates an inflammatory response within the tendon sheath; however, no observable inflammatory response appears to be initiated within the tendon. To our knowledge, there have been no biopsy reports of any tendon in patients with a first episode of acute tendinitis. All published pathologic studies have dealt with biopsies of those with chronic tendinitis or biopsies of
BICEPS TENDON Lesions of the biceps tendon are not infrequent about the shoulder, whether related to a single traumatic incident, repetitive microtrauma, or impingement. These lesions can 283
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be divided into three main categories—bicipital tendinitis, primary or secondary, instability of the biceps tendon (subluxation or dislocation), and biceps tendon rupture. DePalma and Callery11 have reported biceps tenosynovitis as the most common cause of shoulder pain and found that it usually coexists with frozen shoulder. Barnes and Tullos12 have reported five cases of bicipital tendinitis and three cases of subluxation of the biceps long head tendon in 56 painful shoulders in baseball players, reiterating its common cause of the painful shoulder. Occasionally, patients with superior labral anterior-posterior (SLAP) lesions, partial- to full-thickness rotator cuff tears, or both, present with biceps tendon pain.
Functional Anatomy of the Biceps The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula and from the superior glenoid labrum of the shoulder joint. The tendon traverses the glenohumeral joint through a synovial extension of the shoulder and leaves the joint in the intertubercular groove deep to the transverse humeral ligament. The muscle then joins the short head arising from the coracoid process and extends down the humerus before reaching a common insertion on the bicipital tuberosity of the radius.13,14 The nerve supply emanates from the musculocutaneous nerve derived from a coalescence of the fifth and sixth cervical nerve roots. The long head appears to assist in depression of the humeral head and further aids in the stabilization of the humeral head in the glenoid. The biceps muscle is important in flexion and supination of the forearm, performing maximally with the elbow flexed at 90 degrees. Cadaveric studies15 have shown that the long head is important in preventing upward migration of the humeral head when the short head is contracted. Kumar and associates15 have noted that an absent long head tendon would allow upward migration of the humeral head when the short head is stimulated; this is believed to be important in fine positioning of the head in the glenoid to improve elbow flexion and supination power. Studies by Rodosky and coworkers16 have noted that the biceps contributes to shoulder stability by resisting external rotation forces that occur in the abducted, externally rotated position, as occurs during the late cocking phase of throwing. Electromyographic studies by Jobe and colleagues17,18 in throwers have noted modest intensity during the cocking phase, with a lessening of activity until ball release, and peak activity occurring during the follow-through phase. The activity is believed to be closely associated with elbow motion (deceleration and forearm pronation) during follow-through and to be important in preventing hyperextension of the elbow.17-20
Biceps Tendinitis Although biceps tendinitis is not uncommon, it is not known whether this is an isolated entity or whether it exists secondary to some other shoulder pathology. DePalma
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and Callery11 have reported biceps tendinitis as the most common cause of shoulder pain, and early literature is replete with articles on the diagnosis and treatment of the primary entity. Neer21-23 has noted the potential for biceps tendinitis in those with impingement and has indicated that biceps tendinitis may be an early sign of impingement. It is our experience that both conditions exist, and we concur with Post and Benca24 that primary biceps tendinitis represents about 5% of all clinical cases. In most cases, the biceps tendinitis appears secondary to mechanical or chemical irritation. Clinical Presentation Typically, the patient will complain of anterior shoulder pain, usually with activity. This may be insidious in onset, follow a single traumatic incident or, as usually occurs in the athletic population, frequently occurs as an overuse phenomenon as a consequence of repetitive microtrauma or secondary to impingement. It may occur as an isolated entity but usually is secondary to some other pathologic process. It is important to note the presence of other shoulder pathologies, particularly rotator cuff pathology, glenohumeral instability,25 impingement, or generalized inflammatory conditions of the shoulder as the cause. We believe that in those patients with chronic rotator cuff tendinitis, the long head of the biceps acts in a prolonged fashion to depress and steer the humeral head and provide more room for the inflamed bursa and cuff. Thus, these patients will be more susceptible to the development of a painful tendinitis-type syndrome. The most common physical examination finding is tenderness to palpation over the bicipital groove.11,24,26,27 Speed’s test26,28 is performed by flexing the shoulder against resistance while the elbow is extended and forearm supinated. A positive test localizes pain to the bicipital groove. Yergason’s sign28,29 is positive when biceps pain results from supination against resistance with the elbow flexed. Both tests can be helpful but are often nonspecific.23 The relation of bicipital tendinitis and frozen shoulder has been described11,26 and must be taken into account during the examination. Also, the possibility of cervical pathology in the patient with shoulder pain and a paucity of physical examination findings must be remembered. Radiographic Evaluations Although radiographs are believed to be of little value,24 several abnormalities have been reported to be associated with biceps tendinitis, including the presence of a supratubercular ridge and shallow bicipital grooves27,30 and any osteophyte or spur formation in or near the groove.11,29 Ahovuo and associates31 have noted that plain radiographs reveal degenerative changes in the walls of the grooves in 50% of patients with bicipital tendinitis. They also indicated that arthrography is helpful for those with dislocated biceps tendons, but that there is no difference in filling of the tendon sheath in patients with surgically verified
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tendinitis compared with those with normal tendons. They also reported on the accuracy of sinography in discerning biceps tendon position and noted that this is a useful technique when the sheath is not visualized by arthrography.32 Magnetic resonance imaging (MRI) has proved useful in delineating the different pathologic entities that may be present in patients with rotator cuff symptoms.33,34 It has proved as accurate as ultrasound for evaluating rotator cuff tendinitis and tendon disruption but is more accurate for diagnosing biceps tendon dislocation.35 Pathology DePalma and Callery11 have reported on gross and microscopic pathologic findings in 86 symptomatic shoulders, noting isolated biceps tendon involvement in 62%; in 38%, this was found to be secondary to a more generalized inflammatory process. The essential pathology is of varying intensity and involves the tendon sheath complex. Grossly, the outer synovial sheath is hemorrhagic and constricted on either side of the transverse humeral ligament. Microscopically, edema, collagen degeneration, increased vascularity, and round cell infiltration are noted. In an operative procedure for refractory bicipital tenosynovitis, Michele29 has noted that an adhesive inflammatory process may actually attach the tendon to the groove, diminishing the effect of the gliding mechanism. In patients diagnosed with bicipital tenosynovitis, Crenshaw and Kilgore26 have noted capillary dilation, edema, and cellular infiltration in acute cases, with tendon fraying, narrowing, and fibrosis in chronic cases. In general, pathologic processes are believed to parallel the duration and severity of clinical symptoms.11,29 In 13 inflammatory tendons in which tenodesis was performed, Dines and coworkers36 have noted varying degrees of inflammation; adhesions and synovitis were found in all patients, with only one grossly irregular groove. In patients with chronic tendinitis, Becker and Cofield9 have noted gross tendon abnormalities in 32 of 38 tendons; however, in contrast to other histologic studies, most tendons were normal, and only one had evidence of tendon inflammation. Biceps Tendon Subluxation and Dislocation Biceps tendon dislocation typically occurs medially, as originally described by Meyer.30 It may occur after a specific traumatic incident, such as a tuberosity fracture, or on a chronic basis associated with rotator cuff pathology. Neer23 has noted that this is unusual in patients younger than 40 years unless in association with a fracture. Clinically, there is no pathognomonic sign,37 but the test of Abbott and Saunders38 may help differentiate biceps tendon dislocation from tendinitis. The test is performed by placing the patient’s arm in full abduction and external rotation, and then slowly brought down to the side. A palpable, audible, or painful click may be felt or heard, which strongly suggests the diagnosis. Frequently, however, the patient will complain of pain and a feeling of snapping in the anterior shoulder. The definitive diagnosis of a subluxating biceps tendon is difficult to make based on examination findings
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but arthrography, ultrasound, and MRI are all helpful in identifying the chronically dislocated tendon. DePalma and Callery11 have reported seven cases of subluxation and dislocation. They discerned the tendon slipping in and out of the groove with abduction and external rotation. Dines and colleagues36 have also reported seven cases diagnosed at the time of biceps tenodesis for localized anterior shoulder pain over the bicipital groove. In cadaveric studies, Slatis and Aalto37 have found that the most important ligament for stabilization is not the transverse humeral ligament but the medial portion of the coracohumeral ligament. Transection of the transverse humeral ligament does not affect stability of the biceps tendon. They also reported five cases of medial dislocation and four cases of subluxation in live patients. In the dislocation patients, the biceps tendon was found displaced medially, lying on the superficial aspect of the subscapularis; they were noted to have associated supraspinatus tears, with involvement of the coracohumeral ligament. The tendon was located in a fascial sling on the ventral aspect of the subscapularis tendon. The four patients with subluxating tendons had limited cuff lesions, and these tendons were located in the groove. Good results were obtained in eight of nine patients when treated by tenodesis and rotator cuff repair when indicated. Petersson39 has reported an incidence of medial dislocation of 6.5% in 77 autopsy dissections. Dislocation was always found to be associated with full-thickness supraspinatus tendon ruptures and with partial- or full-thickness subscapularis tears, allowing the tendon to dislocate deep to the subscapularis muscle. Paulos and associates40 have reported on three unstable tendons after shoulder injuries that usually consisted of a combined distal arm traction and biceps contraction, or a forceful biceps contraction alone, in athletic activity. Two were dislocated superficial to an intact subscapularis and one deep to a partially ruptured subscapularis. Two main mechanisms of dislocation have been described; they generally occur in concert with rotator cuff pathology. The tendon dislocates medially and lies superficial to the subscapularis after coracohumeral ligament rupture, or dislocates after undersurface subscapularis rupture in which the superficial fibers stay attached to the transverse humeral ligament, allowing the tendon to dislocate medially and deep to the subscapularis muscle. Tenodesis is believed to be the treatment of choice, combined with rotator cuff reconstruction when indicated. Nonoperative Rehabilitation Approach The nonoperative treatment of biceps pain is based on the recognition and classification of the pathology. Thus, a differential diagnosis is critical to a successful outcome. We have found biceps pain to have several different causes (Box 23-1).
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BOX 23-1.
• • • • • • •
Potential Causes of Biceps Pain
Biceps tendon instability Peritendinitis (tendinitis) Tendinosis Glenohumeral joint hypermobility Capsular inflammation SLAP lesions Rotator cuff failure
SLAP, superior labral anterior-posterior.
The most common cause of this pain response is tendinosis or tendinitis of the biceps brachii long head tendon. The differential diagnosis is based on the patient’s history (e.g., chronicity of pathology, number of episodes), nature of the pain, elasticity and flexibility of the tendon, and MRI findings. Patients with peritendinitis present with acute onset, no or minimal previous history of symptoms, mild stiffness, and MRI findings that indicate inflammation of the paratenon.5 The treatment of paratendinitis is cryotherapy,41 nonsteroidal anti-inflammatory drugs (NSAIDs), iontophoresis with dexamethasone,42-45 and moderateintensity exercise. The patient is encouraged to restore flexibility and perform light strengthening exercises. The goal of the program is to reduce inflammation, so aggressive exercise is contraindicated. We use the disposable iontophoresis patch (Empi Medical, St. Paul, Minn) for the treatment of biceps paratendinitis (Fig. 23-1). Conversely, the treatment for biceps tendinosis is dramatically different. Its goal is to produce a healing response to the degenerative tendon by increasing circulation to the tendon. Treatment measures include heat, ultrasound, transverse massage, cross-friction massage, eccentric muscle training, flexibility exercises, and a progressive loading program to allow the tendon to respond to the stress. The purpose of the eccentric training is to load the tendinous and musculotendinous junction rather than the muscle belly. The exercise should be progressive in nature, with the goal of loading the tendon to produce collagen synthesis and organization.46 Another cause of biceps tendon pain is capsular inflammation, synovitis, or both. This can be seen in the early stages (I and II) of adhesive capsulitis (see Chapter 24). As noted earlier, with adhesive capsulitis, the biceps tendon sheath often becomes involved, resulting in biceps tenosynovitis.11,29,36 We recommend treating these patients for inflammation with NSAIDs, cryotherapy, iontophoresis, and gentle exercise. During the synovitisinflammatory stage, we encourage frequent bouts of light range-of-motion (ROM), stretching, and flexibility exercises (see Chapter 24 for specific details.)
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Figure 23-1. Disposable iontophoresis patch (Empi Medical, St. Paul, Minn). This patch is used for the treatment of biceps paratendinitis.
Other types of glenohumeral joint lesions that can cause biceps pain include rotator cuff pathologies (e.g., impingement, tendinitis, failure), glenohumeral joint hypermobility, and SLAP lesions. The clinician is encouraged to treat each pathology specifically based on the differential diagnosis.
Long Head Tendon Ruptures Petersson39 has reported 6 cases of long head tendon rupture in 153 cadaver shoulders. In most cases, this is believed to occur in patients older than 40 years23 with a history of shoulder pain suggesting a preexisting rotator cuff lesion. Carroll and Hamilton47 have reported an average age of 51 years in their series of 54 long head ruptures. Rarely does a long head rupture occur in an individual before the fourth decade. If it does, it is frequently the result of a single traumatic incident and may occur at the musculotendinous junction.25 A mechanism of traumatic injury has been described as a forceful biceps contraction during athletic maneuvers with biceps contraction combined with arm traction (gymnastics),40 or the result of a sudden biceps contraction with the arm in external rotation abduction. Neer23 has described three types of biceps long head ruptures that usually occur at the cephalad aspect of the groove. These include rupture with retraction,
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in which the diagnosis is often easily made based on swelling, pain, and the sudden appearance of a “Popeye” muscle. Rupture may also occur with partial recession or self-attachment to the groove or transverse ligament, which makes the diagnosis more difficult because of lack of deformity. We have noted an occasional patient with chronic rotator cuff tendinitis in whom the symptoms are relieved, at least initially, after rupture of the long head. Isokinetic strength testing at 2 years after rupture in 10 patients has revealed no significant loss of elbow flexion strength and only a 10% decrease in elbow supination strength.25 Sturzeneggar and colleagues48 have used isokinetic testing to compare strength in the conservatively treated long head biceps tendon rupture with that in the surgically treated (tenodesis) group; they found that strength decreases by 16% in elbow flexion in the nonoperative group versus 8% in the surgical group. Comparing supination, strength was decreased 11% in the conservative group and 7% in the surgical group. Interestingly, a slight strength loss (4%) of shoulder abduction was noted in the surgical group. There have been reports of rotator cuff tears coexisting with biceps ruptures.22,25 Usually the supraspinatus tear precedes the biceps rupture. As noted, treatment is based on several factors, the most important of which is the presence of preexisting shoulder pain. If pain is present prerupture, an arthrogram is indicated to rule out associated rotator cuff tear. If the arthrogram reveals a tear and pain persists, cuff repair, acromioplasty, and biceps tenodesis are performed. If the arthrogram is negative and the patient accepts the Popeye muscle, nonoperative treatment is indicated. If the patient does not like the cosmetic deformity, tenodesis, acromioplasty, and exploration of the rotator cuff are indicated. Early tenodesis is usually considered for the young athlete only after an acute traumatic incident. Burkhart and Fox49 have reported two cases of long head tendon rupture in young patients associated with significant intra-articular pathology, including labral tears. A loose body and retained biceps tendon stump, resulting in grade IV chondromalacia of the glenoid, were noted in one. Arthroscopy was recommended after acute rupture when surgical tenodesis is chosen or for those patients with persistent symptoms after nonoperative management to rule out significant intra-articular pathology. Recommended Treatment It is our contention that actual cases of primary bicipital tendinitis are rare and that most cases are secondary to underlying shoulder pathology, such as chronic rotator cuff tendinitis, SLAP lesions, or instability. Although biceps tendinitis may be the most prominent symptom at any time during the disease course, careful evaluation of the rotator cuff is mandatory. Conservative treatment consists of a comprehensive exercise program and a short course of oral NSAIDs. Selective injections with a 1% lidocaine and dexamethasone (Decadron) mixture are helpful
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therapeutically and diagnostically. These may be delivered into the subacromial space or biceps tendon sheath or groove, avoiding direct injection of the tendon. Rehabilitation programs to treat the rotator cuff pathologies may be beneficial. Modalities such as iontophoresis42 and cryotherapy have been successful. Performing isolated biceps tenodesis is rarely indicated, with the exception of the previously operated shoulder in which the patient has failed an adequate decompression and continues to have pure shoulder pain consistent with biceps tendinitis. Kelly and associates50 have reported excellent results in 77% of patients who exhibited biceps pain with a biceps tenotomy. The other side effects noted were cosmesis and elbow flexor cramping with exertion. It may be indicated to perform a biceps tenodesis or to make several longitudinal incisions in the long head tendon. These may be carried out in the hope of stimulating a healing response in those with persistent symptoms suggestive of biceps tendinitis, despite being adequately treated for rotator cuff tendinitis with a nonoperative regimen, or in those undergoing arthroscopic decompression. Subluxating or dislocating long head biceps tendons are not common clinically, particularly in the young, active athletic population. This usually occurs in combination with rotator cuff tears and, if tenodesis becomes necessary, it is usually combined with decompression and rotator cuff reconstruction. Although long head ruptures are also rare in the young athlete, an aggressive surgical approach is indicated for some of these patients. In the older athlete, long head ruptures are usually treated early with oral NSAIDs and an aggressive functional rehabilitation program. However, in patients with persistent shoulder pain or weakness, an arthrogram or MRI scan should be obtained; if a partial- or full-thickness rotator cuff tear exists, an arthroscopic evaluation, rotator cuff repair, tenodesis, and acromioplasty should be considered.
PECTORALIS MAJOR RUPTURES Anatomy and Function The pectoralis major originates from the clavicle and sternum, courses laterally, and is invested by the pectoral fascia as it forms the anterior axillary fold. It has clavicular, sternocostal, and abdominal portions; the sternocostal is the largest. The fibers converge to insert on the crest of the greater tuberosity of the proximal humerus.13,14 The muscle functions in flexion and adduction and assists in internal rotation of the humerus and, to a lesser extent, elevation and depression of the shoulder. Marmor and colleagues51 have studied strength differences between arms in a patient with a congenital absence of the pectoralis major, noting the primary strength loss in adduction and internal rotation of the humerus. Innervation is by the lateral and
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medial pectoral nerves. Electromyographic studies of the throwing shoulder17,18,52 report that the pectoralis major becomes active in the late cocking phase, when external rotation reaches its maximum. Activity continues in the muscle in concert with the latissimus dorsi during the acceleration phase (internal rotation and adduction); activity decreases during follow-through. The pectoralis major is of primary importance in producing ball velocity.52
Causative Factors Marmor and associates51 have noted that pectoralis major ruptures are rare. They postulated that because of its unique anatomy, rupture must be a result of trauma to a normal tendon. They studied load velocity curves in healthy muscles and found that muscle can hold four times as much as it can lift. They postulated that rupture in a healthy athlete is caused by application of excessive weight when the muscle is already holding at its maximum power. As reported by McMaster,53 under heavy loads, rupture would occur at the tendon insertion or musculotendinous junction and not through a healthy tendon. The age range reported is from infancy to 72 years54; The median age, excluding infants, is 30 years, with a peak age between 20 and 30 years. The most common cause of rupture is improper muscle coordination during heavy lifting, as occurs during violent involuntary contractions caused by excessive muscle tension; in two studies, all patients were male.54-56 Complete ruptures usually occur at the tendinous insertion. Partial ruptures may occur at the musculotendinous junction or within the muscle belly itself.49 Tendinitis of the pectoralis major insertion is no doubt more common than rupture but, because of the benign nature of the injury and excellent response to nonoperative treatment, few studies have been done.
present. Effort to contract against resistance is painful and accentuates the defect. A visible palpable defect in the lower fibers of the pectoralis muscle adjacent to the deltopectoral interval may be present, but this is not believed to be a reliable sign, because a fascial covering may remain intact and feel remarkably similar to an intact tendon.56 The most reliable clinical test is to have the patient place both hands on his or her lateral iliac crest and then push inward (Fig. 23-3). One can then readily palpate the combined tendon of the sternal and clavicular portions and compare it with the opposite noninjured side. Partial ruptures, although not common, appear in our experience to be equal to complete ruptures in incidence (Fig. 23-4). This latter entity is often missed or misdiagnosed but, with the clinical tests described earlier, is more easily discovered. Chest x-ray may show a loss of the normal axillary tendon shadow.51,54,56 MRI may prove to be the best available diagnostic test in the future.
Figure 23-2. Patient referred with a presumed diagnosis of proximal long head of biceps rupture based on location of the ecchymosis. This location is commonly seen in pectoralis major ruptures.
Chadwick57 has reported two cases of insertional tendinitis manifesting as a suspicious humeral lesion at the insertion site, necessitating biopsy. Pathology was consistent with benign inflammation and tendon degeneration, indicating that the diagnosis does exist. Whether insertional tendinitis or tendinosis is a common precursor to rupture is a matter of conjecture.
Presentation The typical presenting complaint is a sudden sharp pain in the upper arm or shoulder53 during an exertional athletic maneuver or a fall. An audible snap or pop may be heard.55 On examination, ecchymosis is common over the lateral chest wall, axilla, or proximal humerus (Fig. 23-2). Hemorrhage may occur almost entirely over the area of the biceps muscle, suggesting a possible proximal biceps rupture, particularly when the individual has pain with resisted arm flexion. A bulge of the anterior chest wall on flexion and pain and weakness on adduction internal rotation are
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Figure 23-3. Asymmetrical pectoralis major muscles consistent with partial rupture. A complete rupture usually shows a more dramatic asymmetry.
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289
SNAPPING SCAPULA SYNDROME
Figure 23-4. Palpation of the pectoralis major tendon. This is key to a successful examination.
Treatment Although satisfactory results can be obtained in the non– high-profile, non–weight-lifting athlete with nonoperative treatment, surgical repair is otherwise necessary and has been proved successful.54-56 The chosen method of treatment depends not only on the activity level and age of the patient, but on the location of the tear and the ability of the patient to accept a cosmetic defect. Proximal injuries at the muscle tendon junction—probably rare—respond favorably to nonoperative treatment, but distal lesions are best treated surgically.56 Zeman and coworkers56 have reported on nine ruptures. The average patient age was 30 years. Seven were believed to be caused by excessive muscle tension. The five patients treated nonoperatively could not return to their previous athletic activity levels, but the four patients treated surgically had excellent results and all were able to return to their prior activity levels. Kretzler and Richardson58 have reported operative treatment of 16 ruptures treated up to 5.5 years postinjury. All 16 had good pain relief; 13 reported full, subjective strength return. Recommended Treatment Our experience is consistent with that of others in that most ruptures occur during violent muscle contraction, such as bench pressing or lifting heavy objects. The diagnosis can usually be made on the basis of a typical history and physical examination findings, although MRI may prove helpful in difficult cases. We are aggressive in recommending repair for the young athletic population. Most tears occur at the tendinous insertion and are readily repaired to the original insertion sites through a bony trough, with consistently good results. Bone-implanted suture devices can facilitate the repair process.
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This uncommon but significant disorder affecting the shoulder region is frequently confused with myofascitis and seldom recognized. The scapula is the site of origin of rotator cuff musculature, and the scapulothoracic joint is an important contributor to shoulder motion. As noted by Milch,59 the snapping scapula is not uncommon but is usually neglected; patients are often described as neurotic and are rarely referred to an orthopedist for evaluation. Causes of the snapping scapula are believed to include an abnormal superior scapular angle, tumorous conditions, particularly osteochondromas, and changes consistent with interstitial fibrosis in the surrounding musculature.32 A series of five cases resulting from subscapular exostoses has been reported.60 Four cases caused by scapulothoracic bursitis at the inframedial scapular border in professional baseball pitchers have been reported.61 Three subsequent cases at the superior medial angle have been described in manual laborers, citing repetitive trauma as a possible cause.62 It has been our experience that the undersurface of the superior medial angle may be more rounded and somewhat thicker than normal, subsequently rubbing over the posterior upper thoracic ribs to produce a painful bursitis, and perhaps a periostitis.
Clinical Presentation The patient usually presents with neck pain but, on questioning, can pinpoint the pain to the general area of the insertion of the trapezius and rhomboid muscles at or near the superior angle of the scapula. Often, the patient may also complain of a painful snapping or grating over the superior medial scapular angle. These symptoms are made worse with overhead rotation of the arm, which produces scapular compression over the posterior ribs. On physical examination, the painful area can usually be localized to this area, and often a palpable audible snapping or popping sensation can be elicited, particularly when the examiner applies compression to the superior scapula during the overhead motion. This frequently will produce a grating sound, which may be caused by compression of the bursa or by the scapula grating over the ribs. This can usually be differentiated from myofascitis (trigger point) in that the maximal area of tenderness is not at the scapular angle but is localized to a small area in the trapezius muscle in the case of myofascitis. A local injection of xylocaine or bupivacaine (Marcaine) under the superior medial edge of the scapula should render the area almost completely asymptomatic, even with overhead motion and compression applied to the superior medial angle of the scapula. Plain radiographs are usually normal.61 The importance of obtaining oblique views60 and a computed tomography (CT) scan62 have been reported; CT scanning is now the procedure of choice, particularly when bony lesions are suspected.
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Treatment This syndrome is occasionally seen in pitchers, throwers, and golfers acutely or subacutely. Initial treatment consists of differentiating it from the more commonly occurring muscle strain and myofascitis. If the diagnosis is consistent with snapping scapula, the primary entity is probably a bursitis, and treatment consists of active rest, combined with oral NSAIDs and occasional injections. In resistant pain, particularly if the problem is secondary to an exostosis, surgical treatment can be offered. Milch59 has reported that simple removal of small parts of the scapula will predictably result in a cure. Surgical Therapy Parsons60 has reported four cases resulting from exostoses that were successfully treated surgically. Sisto and Jobe61 have reported four bursal excisions at the inferomedial angle, allowing four professional pitchers to return to their prior levels of competition. Richards and McKee62 have reported three successful outcomes after resection of the superior medial angle of the scapula in laborers, and Arntz and Matsen63 have reported satisfactory outcomes in 12 of 14 patients after superior medial angle resection. Nonoperative Treatment The nonoperative treatment of snapping scapula is focused on correcting the patient’s postural adaptations after patients exhibit anterior tilting and retracted posture. Stretching and strengthening exercises are encouraged. The purpose of this program is to reduce the inflammation of the bursa and restore mobility of the scapulothoracic joint through soft tissue and joint mobilization techniques. The patient is encouraged to restore proper posture with an emphasis on scapular refraction, posterior tilting, and external rotation. Stretching of the pectoralis minor and major is performed with scapular refraction and posterior tilting exercises. Physiotaping, bracing, or both may be beneficial. The patient is encouraged to perform rotator cuff and shoulder strengthening exercises. The patient is instructed to restore shoulder motion but not perform repetitive work or sport movement over the head, allowing the inflammation to reduce. Recommended Treatment We have seen several cases, usually of a chronic nature, within the past several years. None of these patients had an exostosis or osteochondroma. Initial treatment consists of rest, oral anti-NSAIDs, and injections. Proper injection technique is important because of the proximity to the posterior thoracic wall and pleural cavity. After applying a sterile preparation, a 22-gauge 1.5-inch needle with 1% lidocaine and dexamethasone is introduced, angling from cephalad to caudad at a 45-degree angle just off the superior medial tip of the scapula, because the bursa is usually approximately 2 cm lateral to the superior medial angle.
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Conservative treatment consists of gentle active assisted ROM exercises and isometric shoulder and scapular strengthening, progressing to isotonic strengthening. Once the patient has accomplished full nonpainful motion and strength equal to those of the opposite side, a return to sport is allowed. If conservative treatment fails, surgery is indicated if so desired by the patient. The technique62 consists of making a curved 4-cm incision over the superior medial angle. The fascia is divided longitudinally and the trapezius is split in line with its fibers. The levator and subscapularis attachments are elevated subperiosteally off the angle. A large malleable retractor is placed beneath the tip to protect the posterior chest wall. A 1-inch osteotome is used to remove the tip, which consists of a 3- ⫻ 1.5-cm area of bone. The edges are trimmed with a rongeur and the bursal tissue is excised. The wound is closed in routine fashion. The results are predictably good in our limited experience. Early functional rehabilitation is begun immediately postsurgery, and it is essentially similar to that used for an arthroscopic shoulder decompression.
QUADRILATERAL SPACE SYNDROME The quadrilateral space is defined as the area bounded medially by the long head of the triceps, laterally by the humerus, superiorly by the teres minor, and inferiorly the teres major, through which pass the axillary nerve and posterior circumflex humeral artery.14 Quadrilateral space syndrome was originally described by Cahill and Palmer64 in 1983. The syndrome typically occurs in young active adults between the ages of 22 and 35 years. It usually is not associated with any history of shoulder trauma. A patient complains of insidious onset of pain and nondermatomal, nonradiating paresthesias in the involved shoulder. A throwing athlete may complain of early fatigue, weak abduction, a numb shoulder, or dead arm– type syndrome.64 Physical examination reveals tenderness consistently over the involved quadrilateral space, and symptoms may be reproduced with abduction and external rotation of the arm. The cause is believed to be tethering of the neurovascular structures by obliquely oriented fiber bands in the quadrilateral space. Electromyographic and nerve conduction velocity studies are not helpful in making the diagnosis and are usually normal. Arteriographic evidence of posterior circumflex arterial occlusion and the associated axillary nerve compression, combined with a typical history and physical examination findings, are believed to be diagnostic. The importance of proper angiographic technique to visualize the posterior circumflex humeral artery with the arm at the side and in the abduction–external rotation position has been stressed.65 As noted by Cahill and
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Palmer,64 70% of patients in their series had symptoms that did not warrant surgery, and alteration of pitching mechanics may prove beneficial in symptom relief. In those resistant to nonoperative treatment methods, 18 patients were treated surgically; 16 of 18 improved with surgical decompression.
SUMMARY There are numerous soft tissue lesions about the shoulder that can cause the patient to experience significant shoulder pain. Most of these lesions can be successfully treated with nonoperative treatment regimens. The team approach—the team is comprised of the physician, physical therapist, and athletic trainer—is critical for successful treatment. The differential diagnosis must be communicated to the treatment team; a specific and differential diagnosis is vital to successful treatment. Based on the differential diagnosis and identification of all involved tissues, a well-designed rehabilitation program must be established. If the nonoperative approach fails and does not meet the functional demands of the patients, surgical intervention may be indicated. Nonoperative and operative treatment modalities have been discussed in this chapter.
References 1. Ryan GB: Inflammation.. Kalamazoo, Mich, Upjohn, 1977. 2. Schurman DJ, Goodman SB, Smith RL: Inflammation and tissue repair. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): Sports-Induced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990, pp 277. 3. Hargreaves KM: Mechanisms of pain sensation resulting from inflammation. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): Sports-Induced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990, pp 383. 4. Clancy WG Jr: Specific rehabilitation for the injured recreational runner. Instr Course Lect 38:483, 1989. 5. Clancy WG Jr: Tendon trauma and overuse injuries. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): SportsInduced Inflammation. American Academy of Orthopaedic Surgeons, Chicago, 1990, pp 609. 6. Clement DB, Taunton JE, Smart GW: Achilles tendinitis and peritendinitis: Cause and treatment. Am J Sports Med 12:179, 1984. 7. Nirschl RP: Patterns of failed healing in tendon injury. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): SportsInduced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990. 8. Nirschl RP: Rotator cuff tendinitis: basic concepts of pathocause. Instr Course Lect 38:439, 1989. 9. Becker DA, Cofield RH: Tenodesis of the long head of the biceps brachii for chronic bicipital tendinitis. J Bone Joint Surg Am 71:376, 1989. 10. Puddu G, Ippolito E, Postacchini F: A classification of achilles tendon disease. Am J Sports Med 4:145, 1976.
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11. DePalma AF, Callery GE: Bicipital tenosynovitis. Clin Orthop 3:69, 1954. 12. Barnes DA, Tullos HS: An analysis of 100 symptomatic baseball players. Am J Sports Med 6:62, 1978. 13. Netter F: The Ciba Collection of Medical Illustrations, vol 8, part 1. Anatomy of the Musculoskeletal System. West Caldwell, NJ, Ciba-Geigy, 1987. 14. Romanes GJ: Cunningham’s Textbook of Anatomy. New York, Oxford University Press, 1981. 15. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop 244:172, 1989. 16. Rodosky MW, Harner CD, Rudert MJ, et al: The role of the biceps-superior glenoid labrum complex in anterior stability of the shoulder. Orthop Trans 15:58, 1991. 17. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. Am J Sports Med 11:3, 1983. 18. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching—a second report. Am J Sports Med 12:218, 1984. 19. Abrams JS: Special shoulder problems in the throwing athlete: Pathology, diagnosis, and nonoperative management. Clin Sports Med 10:839, 1991. 20. Andrews JR, Carson WG Jr, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. 21. Neer CS II: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg Am 54:41, 1972. 22. Neer CS II: Impingement lesions. Clin Orthop 173:70, 1983. 23. Neer CS II: Cuff tears, biceps lesions, and impingement. In Neer CS II (ed): Shoulder Reconstruction. WB Saunders, Philadelphia, 1990, pp 62-__. 24. Post M, Benca P: Primary tendinitis of the long head of the biceps. Clin Orthop 246:117, 1989. 25. Warren RF: Lesions of the long head of the biceps tendon. Instr Course Lect 34:204, 1985. 26. Crenshaw AH, Kilgore WE: Surgical treatment of bicipital tenosynovitis. J Bone Joint Surg Am 48:1496, 1966. 27. Hitchcock HH, Bechtol CO: Painful shoulder—observations on the role of the tendon of the long head of the biceps brachii in its causation. J Bone Joint Surg Am 30:263, 1948. 28. Simon WH: Soft tissue disorders of the shoulder—frozen shoulder, calcific tendinitis, and bicipital tendinitis. Orthop Clin North Am 6:521, 1975. 29. Michele AA: Bicipital tenosynovitis. Clin Orthop 18:261, 1960. 30. Meyer AW: Spontaneous dislocation of the tendon of the long head of the biceps brachii. Arch Surg 13:109, 1926. 31. Ahovuo J, Paavolainen P, Slatis P: Radiographic diagnosis of biceps tendinitis. Acta Orthop Scand 56:75, 1985. 32. Ahovuo J, Paavolainen P, Slatis P: Diagnostic value of sonography in lesions of the biceps tendon. Clin Orthop 202:184, 1986. 33. Iannotti JP, Zlatkin MB, Esterhai JL, et al: Magnetic resonance imaging of the shoulder. J Bone Joint Surg Am 73:17, 1991. 34. Nelson MC, Leather GP, Nirschl RP, et al: Evaluation of the painful shoulder. J Bone Joint Surg Am 73:707, 1991. 35. Vellet AD, Munk PL, Marks P: Imaging techniques of the shoulder: Present perspectives. Clin Sports Med 10:721, 1991.
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36. Dines D, Warren RF, Inglis AE: Surgical treatment of lesions of the long head of the biceps. Clin Orthop 164:165, 1982. 37. Slatis P, Aalto K: Medial dislocation of the tendon of the long head of the biceps brachii. Acta Orthop Scand 50: 73, 1979. 38. Abbott LC, Saunders JB: Acute traumatic dislocation of the tendon of the long head of the biceps brachii. A report of six cases with operative findings. Surgery 6:817, 1939. 39. Petersson CJ: Spontaneous medial dislocation of the tendon of the long biceps brachii—an anatomic study of prevalence and pathomechanics. Clin Orthop 211:224, 1986. 40. Paulos LE, Grauer JD, Smutz WP: Traumatic lesions of the biceps tendon, rotator cuff interval, and superior labrum. Orthop Trans 15:85, 1991. 41. Knight KL: Cryotherapy: Theory, Technique, and Physiology. Chattanooga, Tenn, Chattanooga Corporation, 1985. 42. Nowicki KD, Hummer CD, Heidt RS, Colosimo AJ: Effects of iontophoretic versus injection administration of dexamethasone. Med Sci Sports Exerc 34:1294, 2002. 43. Bertolucci LE: Introduction of anti-inflammatory drugs by iontophoresis: Double-blind study. J Orthop Sports Phys Ther 4:103, 1982. 44. Delacerda FG: A comparative study of three methods of treatment for shoulder girdle myofascial syndrome. J Orthop Sports Phys Ther 4:52, 1982. 45. Harris PR: Iontophoresis: Clinical research in musculoskeletal inflammatory conditions. J Orthop Sports Phys Ther 4:109, 1982. 46. Langberg H, Ellingsgaard T, Madsen J, et al: Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis. Scand J Med Sci Sports 17:61-66, 2007. 47. Carroll RE, Hamilton LR: Rupture of biceps brachii—a conservative method of treatment. J Bone Joint Surg Am 49:1016, 1967. 48. Sturzeneggar M, Beguin D, Grunig B, Jakob RP: Muscular strength after rupture of the long head of the biceps. Arch Orthop Trauma Surg 105:18, 1986. 49. Burkhart SS, Fox DL: SLAP lesions in association with complete tears of the long head of the biceps tendon: A report of two cases. J Arthrosc Relat Surg 8:31, 1992.
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50. Kelly AM, Drakos MC, Fealy S, et al: Arthroscopic release of the long head of the biceps tendon: Functional outcome and clinical results. Am J Sports Med 33:208, 2005. 51. Marmor L, Bechtol CO, Hall CR: Pectoralis major muscle— function of sternal portion and mechanism of rupture of normal muscles: Case reports. J Bone Joint Surg Am 43: 81, 1961. 52. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789, 1991. 53. McMaster PE: Tendon and muscle ruptures. Clinical and experimental studies on the causes and location of subcutaneous ruptures. J Bone Joint Surg 15:705, 1933. 54. Park JY, Espiniella JL: Rupture of pectoralis major muscle— a case report and review of literature. J Bone Joint Surg Am 52:577, 1970. 55. McEntire JE, Hess WE, Coleman SS: Rupture of the pectoralis major muscle—a report of eleven injuries and review of fifty-six. J Bone Joint Surg Am 54:1040, 1972. 56. Zeman SC, Rosenfeld RT, Lipscomb PR: Tears of the pectoralis major muscle. Am J Sports Med 7:343, 1979. 57. Chadwick CJ: Tendinitis of the pectoralis major insertion with humeral lesions—a report of two cases. J Bone Joint Surg Br 71:816, 1989. 58. Kretzler HH Jr, Richardson AB: Rupture of the pectoralis major muscle. Am J Sports Med 17:453, 1989. 59. Milch H: Partial scapulectomy for snapping of the scapula. J Bone Joint Surg Am 32:561, 1950. 60. Parsons TA: The snapping scapula and subscapular exostoses. J Bone Joint Surg Br 55:345, 1973. 61. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192, 1986. 62. Richards RR, McKee MD: Treatment of painful scapulothoracic crepitus by resection of the superomedial angle of the scapula—a report of three cases. Clin Orthop 247:111, 1989. 63. Arntz CT, Matsen FA: Partial scapulectomy for disabling scapulo-thoracic snapping. Orthop Trans 14:552, 1990. 64. Cahill BR, Palmer RE: Quadrilateral space syndrome. J Hand Surg 8:65, 1983. 65. Redler MR, Ruland LJ III, McCue FC III: Quadrilateral space syndrome in a throwing athlete. Am J Sports Med 14:511, 1986.
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CHAPTER 24 Adhesive Capsulitis
of the Shoulder E. Lyle Cain, Stephen M. Kocaj, and Kevin E. Wilk
Adhesive capsulitis is a condition of global shoulder motion loss that has been referred to by several names, including periarthritis, pericapsulitis, obliterative subdeltoid bursitis, humeroscapular periarthritis, adhesive capsulitis, bicipital tenosynovitis, and “check rein” shoulder. In 1934, Codman described frozen shoulder as a“pattern of glenohumeral stiffness difficult to define, difficult to treat, and difficult to explain from the point of view of pathology.”1 Nevasier later defined adhesive capsulitis as a “chronic inflammatory process involving the capsule, causing a thickening and contracture, which secondarily becomes adherent to the humeral head.”2 The Shoulder and Elbow Society Consensus in 1992 defined frozen shoulder syndrome as a “condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.” Shoulder rangeof-motion deficit may be seen after injury, trauma, or postsurgical conditions; however, the post-traumatic or postsurgical stiff shoulder differs from adhesive capsulitis, which is usually idiopathic in onset. Adhesive capsulitis is global limitation of active and passive glenohumeral motion resulting from contracture and loss of compliance of the glenohumeral joint capsule. It is caused by intra-articular pathology (capsular contracture), whereas post-traumatic or postsurgical motion deficit is generally caused by extra-articular adhesions or pathology and intra-articular adhesions, rather than solely intraarticular capsular thickening as seen in adhesive capsulitis.
typical age at onset is between 40 and 70 years (mean, 56). It occurs in women more often than men and there is a questionable increased occurrence in the nondominant upper extremity. Patient who have sedentary occupations tend to be more at risk than manual laborers. Interestingly, the diabetic population is more frequently afflicted by this condition than their nondiabetic counterparts. It has been suggested that from 10% to 35% of diabetics will experience adhesive capsulitis during their lifetime.7,8 In addition, bilateral disease is also more common in the diabetic population (30%), especially if the patient has been insulin-dependent for longer than 10 years. Adhesive capsulitis syndrome may antedate the onset of diabetic disease in what has been termed limited joint motion syndrome. The age at onset in this population is often earlier than that of the standard population, and it has been commonly associated with the early skin changes pathognomonic of the diabetic process. The pathophysiology of adhesive capsulitis has been described by Rodeo and colleagues9 as being cytokinemediated. In their study, it was found that cytokines such as transforming growth factor  (TGF-) and plateletderived growth factor (PDGF) may play a role. However, it was concluded that “although the etiology of the stiffness that results in capsular fibrosis remains elusive, our understanding of its pathogenesis is increasing.”9
The mainstay of adhesive capsulitis is nonoperative rehabilitation, with a focus on physical therapy. The rehabilitation approach should vary based on the stage of adhesive capsulitis presented by the patients. In this chapter, we will discuss pathogenesis, differential diagnosis, and various treatment options.
In 1995, Bunker and associates10 described the pathology of the adhesive capsulitis as being similar to that found in Dupuytren’s disease. They compared the histologic findings of 12 patients who underwent open capsular release for adhesive capsulitis with those of 6 patients who underwent surgery for Dupuytren’s contracture in the hand. The histologic and immunocytochemical findings showed that the pathologic process is active fibroblastic proliferation, accompanied by some transformation to a smooth muscle phenotype (myofibroblasts). No inflammation and no synovial involvement were found.
CAUSATIVE FACTORS AND PATHOGENESIS The cause of adhesive capsulitis syndrome still remains unclear. Several proposed mechanisms include autoimmune, inflammatory, fibrogenic, and psychogenic origins.2-6 Diseases associated with adhesive capsulitis include diabetes, thyroid disease, rheumatoid arthritis, scleroderma, cardiovascular disease, and regional sympathetic dystrophy.
DIAGNOSIS The diagnosis of adhesive capsulitis syndrome is made clinically. Diagnostic criteria include a history of restricted shoulder motion without a previous major injury or reconstructive surgery and an examination that demonstrates
Adhesive capsulitis syndrome has been reported to have an incidence of 2% to 5% in the general population. The 293
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global shoulder stiffness. Radiologic examination demonstrates normal cartilaginous and periarticular surfaces. Adhesive capsulitis syndrome involves a spectrum of disease that has been characterized by four stages. Stage I, or the painful stage, occurs at the onset and can last up to 3 months. There is pain in the involved extremity with active and passive motion, with normal motion early followed by mild limitation in global motion, including flexion, abduction, and rotation. Examination under anesthesia is normal or shows minimal loss of range of motion. Arthroscopic evaluation shows diffuse synovitis and capsular erythema, with pathology demonstrating hypertrophic and hypervascular synovitis. The main presentation of this stage is synovitis and no capsular tightness; motion loss is caused by pain. Stage I is often misdiagnosed as some other shoulder pathology, most commonly subacromial impingement syndrome. However, surgical treatment with subacromial decompression does not resolve the pain, the patient often loses more motion, and pain worsens postoperatively. Stage II is the adhesion stage and occurs between 3 and 6 months. There is severe pain with active and passive motion. During this phase, pain is present both from synovitis and from the capsule beginning to become adherent to the humerus. Global motion is limited, often with progressive severe loss in all planes. Examination under anesthesia shows limited passive range of motion equal to awake passive and active motion, with a tight capsular end feel and difficulty with attempts to improve the motion passively. Arthroscopy shows diffuse, thick synovitis. Pathology demonstrates hypertrophic and hypervascular synovitis. Stage III is the frozen stage, and occurs between 6 and 12 months. Patients experience pain at the extremes of motion, but have generally recovered from the severe pain of the painful and freezing stages. There is a marked limitation in global motion, with a rigid end point. Examination under anesthesia shows range of motion equal to awake values, with a rigid capsular end feel. Arthroscopy demonstrates fibrotic synovium and pathology demonstrates burned out synovitis and dense scar. Additionally, during this phase, the inferior capsule has loosened it adhesion. Stage IV is the chronic or thawing stage, which occurs between 15 and 24 months. There is a gradual increase in range of motion, with a concomitant decrease in pain. Pathology continues to show a burned out synovitis and dense scar. Because many disorders may manifest with shoulder pain, a thorough physical and shoulder examination will aid in the diagnosis of adhesive capsulitis syndrome. The most important aspect of the physical examination while evaluating a patient for a frozen shoulder is determination of active and passive range of motion of the glenohumeral joint while stabilizing the scapula to prevent scapulothoracic motion.
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During the third stage, active and passive range of motion will be the same, with a rigid end point, whereas many other pathologic shoulder conditions manifest with limited active motion and normal passive motion. It is important to perform a thorough examination of the cervical spine to rule out a source of referred pain that may be manifest in the shoulder. Strength of the rotator cuff and shoulder girdle muscles is generally not affected. However, patients may appear to have weakness at the extremes of motion because of pain. Imaging studies can be an important tool for the diagnosis of adhesive capsulitis syndrome by ruling out other possible causes of shoulder pain. Standard shoulder radiographs can determine the presence of arthritis or prior trauma, which can be a source of pain that leads to decreased joint motion. In addition, cervical spine radiographs are useful for determining a cervical origin of shoulder pain, such as stenosis, degenerative disc disease, arthritis, and fracture. Magnetic resonance imaging (MRI) studies are generally not helpful for demonstrating primary frozen shoulder, but can assist in determining the presence of a rotator cuff tear that may lead to decreased shoulder motion and a secondary frozen shoulder. Later in the process of adhesive capsulitis (stage II or III), MRI may demonstrate global loss of shoulder volume and obliteration of the axillary recess.11
TREATMENT The natural history of adhesive capsulitis syndrome is generally reported to be gradual resolution, with a return of range of motion and a decrease in pain in the involved shoulder. However, several studies have shown that persistent deficits are often seen at long-term follow-up.12,13 Shaffer and coworkers13 have evaluated patients who experienced adhesive capsulitis syndrome at long-term follow-up. They examined 97 patients with primary (idiopathic) frozen shoulders at 7 years’ follow-up. Only 62 patients were available for examination; 60% of them continued to have some restricted range of motion at long-term follow-up, and most of this occurred with external rotation. Mild functional limitations were reported by 11%; none reported limitations greater than mild. Pain resolved at an average of 6 months. The time from onset of symptoms to resolution of pain and stiffness averaged 12 months. Treatment for adhesive capsulitis syndrome should always begin with conservative measures. Clinical decision making plays an important role, because many patients with a frozen shoulder present to their physician with other diagnoses. Patients often have had partial treatment elsewhere and it is sometimes difficult to decide where in the treatment algorithm patient care should begin. A regimen of physical therapy and nonsteroidal anti-inflammatory drugs (NSAIDs) is initiated primarily. The exact physical therapy regimen is discussed later.
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The use of intra-articular steroid injections may be warranted. Reports vary on the results of steroid injections for the treatment of adhesive capsulitis syndrome, but these may be useful for select patients for temporary benefit to allow participation in a stretching program. Steroid injection in diabetics must be used carefully because it can elevate blood glucose levels.
Physical Therapy Rehabilitation The mainstay of treatment of adhesive capsulitis is physical therapy and nonoperative rehabilitation. The treatment of this pathology is based on the accurate identification of the disorder and classification of the stage of adhesive capsulitis. The differential diagnosis of adhesive capsulitis is based on several typical clinical signs and symptoms. Most patients present with a capsular pattern—external rotation is not limited, followed by a limit in abduction, with internal rotation being the least limited.14 Second, patients exhibit a restriction in inferior accessory glenohumeral gliding, followed by an anterior restriction. The patient’s end feel pain and resistance from end feel are also important to determine the stage of adhesive capsulitis.14 Finally, the gold standard, as discussed by Neviaser,4 is an arthrogram. If the inferior capsule is drawn up and adhering to the anatomic neck of the humerus, the differential diagnosis of adhesive capsulitis is made. The approach to treatment for adhesive capsulitis is different than that for a patient who exhibits a stiff and painful shoulder. The nonoperative rehabilitation program is based on the stage of the lesion and characteristics of each stage (Boxes 24-1 and 24-2). Stage I, adhesive capsulitis, is typically identified by the patient exhibiting moderate pain
BOX 24-1. Treatment Based on Stage of Adhesive Capsulitis
Stage I: Preadhesive stage (synovial inflammation, minimal or no limitation of motion) • Easy frequent light motion Stage II: Acute adhesive capsulitis (synovitis, early adhesions) • Sustained stretching—prolonged stretches (light) Stage III: Maturation stage (loss of axillary fold, decreased synovitis) • Inferior capsular stretches, LLLD stretches Stage IV: Chronic stage (mature adhesions, restrictions) • Prolonged LLLD stretching
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BOX 24-2. Specific Treatment Techniques Based on Adhesive Capsulitis Stages
Stage I: Painful Inflammatory Stage • • • • • • • • •
Moist hot packs AAROM with L bar Pendulum exercises Single-plane mobilization (I-III) Soft tissue mobilization Postural exercises, stretching, corrections Stretching techniques (physiologic, CR, HR) Midrange submaximal isometrics Home program (10-12 times daily) • Motion frequently during the day • Light motion
Stage II: Acute Adhesion with Synovitis Stage • • • • • • • • •
Active warm-up AAROM exercises Single-plane, end-range mobilizations (III, IV) Stretching (physiologic, CR, HR) End-range stretching End-range submaximal isometrics Self-capsular stretching Postural corrections and soft stretching Home program (8-10 times daily) • Frequent stretching and ROM exercises • Sustained stretch at end range
Stage III: Maturation Adhesion Stage • • • • • • • • • • •
Heat Active warm-up (AAROM, UBE) LLLD stretch with concomitant superficial heat Aggressive joint mobilization Single multiplanar glides and combined glides Joint mobilization—emphasize inferior glides CR, HR stretching Self-joint mobilization at home Sustained stretching at home (TERT principle) Strengthening (PNF) exercises Home program (4-6 times daily) Keep it moving
Stage IV: Chronic Adhesion Stage • Continue all treatments listed (see above) • During this phase, emphasize • Oblique and multiplanar mobilizations • Sustained LLLD stretching • Use of home LLLD device for 15-min sessions (4 times daily) • Inferior mobilizations • Postural exercises and stretching
AAROM, active-assisted range of motion; CR, contract relax; HR, hold relax; LLLD, low-load, long-duration; PNF, proprioceptive neuromuscular fasciculation; TERT, total end-range time; UBE, upper body ergometer.
LLLD, low-load, long-duration.
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caused by synovitis and a loss of motion because of pain. No mechanical tightness is present. During this stage, the physical therapy treatment plan is focused on reducing inflammation and encouraging the patient to perform light motion of the shoulder frequently during the day. The patient is often placed on NSAIDs and other modalities for pain and inflammation. The patient is instructed to move the shoulder in a light and easy manner to maintain motion, and is encouraged to perform these exercises for 5 to 10 minutes, at least 8 to 10 times daily. Aggressive stretching and exercise are not encouraged because of the synovitis present. Pool, rope and pulley, pendulum, active-assisted range of motion, grades I and II joint mobilization, and passive range-of-motion (ROM) exercises are encouraged. In stage II, adhesive capsulitis, the patient exhibits a restriction of motion secondary to capsular scarring and thickening, and synovitis is still present. During this stage, the program is slightly more aggressive in restoring motion than in stage I; the physical therapist may treat with grades III and IV mobilization to stretch the capsule, slightly more aggressive stretching is performed, and sustained stretching is done at end range (Fig. 24-1). Additionally, the patient may perform all the other exercises listed for stage I. Stage III is characterized by the patient exhibiting a mechanical restriction in motion. The patient’s end feel is often firm and painful. In this phase, the capsule is tightened and adherent to the humerus, and there is a loss of the axillary fold. During this phase, the focus of treatment is to create a stretch that covers a mechanical deformation of the scarred, thickened, and tightened capsule. In this phase, we recommend the use of low-load, long-duration (LLLD) stretches. The characteristics of this type of stretch is to impart a low-intensity stretch for a longer period of time to create deformation of the collagen tissue. Numerous studies
have documented the efficacy of this type of stretch on adhesions.15-19 We perform this stretch with a Thera-Band (Hygenic, Akron, Ohio) or similar device (Fig. 24-2). The patient is instructed to perform this stretch for 12 to 15 minutes, at least four times daily. This uses the TERT principle, total end-range time, whereas McClure has documented that to improve ROM, the patient must spend 60 minutes per day at end range to ensure plastic deformation of collagen.20 LLLD stretches are performed with superficial heat to help promote relaxation.21 Furthermore, the use of multiplanar joint mobilization glides and oblique plane glides is recommended. The focus and purpose of multiplanar glides is to use joint mobilization techniques that combine rotational stress with concomitant translation; thus, collagen is being stretched in more than one plane simultaneously. An example of a multiplanar glide to improve external rotation would be to apply a distraction force and rotate the humeral head into external rotation while gliding anteriorly, with the arm in abduction and external rotation (Fig. 24-3). The joint mobilization techniques are usually described as anterior, posterior, and inferior. The oblique mobilization technique divides the capsule into quadrants (Fig. 24-4A)—anteroinferior, posteroinferior, anterosuperior, and posterosuperior capsular regions. The specific oblique joint mobilization technique to improve external rotation would be to impart a distraction force and glide the humeral head anteroinferiorly, with the arm in external rotation. These techniques have been extremely beneficial for patients with gross restrictions in motion (see Fig. 24-4B). During all phases of treatment for adhesive capsulitis, the patient is encouraged to perform stretches for postural restoration, scapular positioning, and soft tissue mobility. Scapular mobilization, soft tissue mobilization, and stretching exercises are performed. Patients are also instructed to perform low-level strengthening in all phases of treatment. They should perform exercises for both shoulders and, if the contralateral shoulder exhibits tightening during treatment or later, the patient should aggressively attempt to restore mobility to prevent bilateral involvement. Once the adhesive capsulitis condition has been successfully treated, the patient is encouraged to continue a light exercise program for the entire upper extremity, with a focus on ROM, flexibility, posture, and light strengthening exercises.
Manipulation Under Anesthesia When physical therapy alone fails to produce desired results, manipulation under anesthesia (MUA) can be used. It should be considered for patients who are not responding to a stretching program or who are worsening. It is generally performed under interscalene anesthesia. Figure 24-1. Sustained stretch at end range to improve external rotation motion.
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Loew and colleagues22 have reported on 30 patients who underwent MUA; all 30 exhibited acute capsular rupture
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A
C
B
Figure 24-2. Low-load, long duration (LLLD) stretches. A, LLLD stretches with Thera-Band (Hygenic, Akron, Ohio) to improve external rotation. B, LLLD stretches with Thera-Band and superficial heat to improve external rotation. C, LLLD stretches to improve shoulder external rotation using the Joint Active System (JAS, Atlanta).
postmanipulation. The most common area of rupture was the anteroinferior and posterosuperior capsules. Anderson and associates23 have described their findings associated with MUA and reported on 24 patients who underwent premanipulation arthroscopy of the involved frozen shoulder. Diffuse synovitis and dense scarring were noted. The arthroscope was then removed, MUA was performed, and a palpable release was noted. The arthroscope was then reintroduced into the glenohumeral joint and the
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postmanipulation findings were recorded. All patients were noted to have diffuse synovitis; 79% had a rupture at the anteroinferior capsule that had not been ruptured on initial premanipulation arthroscopy. If the adhesive capsulitis being treated occurred after a rotator cuff repair, the amount of rotator cuff healing at the repair site is considered carefully. Motion loss following rotator cuff repair is often caused by intra-articular and
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B
P
S GH L M G H L
PC
A
PB
A
B
AP Figure 24-3. Multiplanar joint mobilization glide for external rotation.
extra-articular (subacromial) adhesions, which differs in cause and treatment from idiopathic adhesive capsulitis. Generally, forward elevation and external rotation in midelevation theoretically relax tension on the repair.
IG
H
L C
A
Contraindications to MUA include no improvement or a worsening ROM after a previous manipulation and significant osteopenia, which represents an increased fracture risk. In addition, long-term insulin-dependent diabetics have demonstrated a decreased benefit from manipulation alone. The patient and surgeon should discuss preoperatively whether to proceed with surgical intervention; the patient must be made aware of the potential for complications, especially fracture of the humerus, and failure to maintain complete motion. The sequence of manipulation in cases of adhesive capsulitis is variable. Generally, we prefer manipulation in forward elevation before rotation (Fig. 24-5). Manipulation should be performed with the surgeon’s hand close to the patient’s shoulder to decrease the moment arm. With constant firm pressure, a palpable and audible release is often appreciated. If crepitant motion does not occur, manipulation is discontinued. After full forward flexion is obtained, gentle external rotation followed by internal rotation is performed. Again, the surgeon’s hands should be close to the glenohumeral joint to minimize the lever arm and risk of humeral fracture (Fig. 24-6). Overly aggressive manipulation can result in soft tissue (rotator cuff tear) or bony (humeral shaft fracture) iatrogenic injury. Complications of MUA include rotator cuff tear, fracture or dislocation of the shoulder, and brachial plexus injury. After a successful manipulation, continuous passive range of motion (CPROM) may be used to maintain motion. Physical therapy is pursued on a daily basis for the first 1 to 2 weeks and home devices can be used to maintain and improve motion. If MUA is initially successful but
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B Figure 24-4. Glenohumeral joint capsule. A, The glenohumeral joint capsule is divided into quadrants. B, An oblique glenohumeral joint glide to improve shoulder external rotation.
motion is lost over the first 3 to 4 weeks, a repeat manipulation is often effective.
Arthroscopic Capsular Release In the setting of a failed MUA or when MUA is contraindicated, arthroscopic release of the shoulder capsule can be performed. We have recently become more aggressive in performing surgical capsular release instead of manipulation alone. The extent of capsule release can be modified and controlled more easily using arthroscopic techniques, depending on preoperative motion loss and capsular tightness. In idiopathic (primary) adhesive capsulitis, motion loss is generally global and release of the anterior, posterior, and inferior capsule is performed.
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A
299
A
B Figure 24-5. Manipulation initiated in forward elevation before rotation. A, Manipulation should be performed with the surgeon’s hand close to the patient’s shoulder to decrease the moment arm. B, Gentle release of the tight capsule with crepitation results in return of passive forward flexion.
Before beginning arthroscopy, a gentle manipulation is performed following the same guidelines as for MUA. A posterior portal is placed and the arthroscope is introduced into the glenohumeral joint. An anterior portal is placed under direct visualization through the rotator interval. Routine glenohumeral arthroscopy is performed. Partial synovectomy is performed at the rotator interval and in the glenohumeral joint for synovitis. The entire soft tissue structure making up the rotator interval is then excised, including the superior glenohumeral ligament and capsule (Fig. 24-7). The postmanipulation arthroscopic findings are noted, as is the partial inferior capsular rupture that often accompanies MUA. This information will guide the surgeon in deciding which additional structures need to be released. The posterior capsule is then released (Fig. 24-8). A combination of arthroscopic punches and electrocautery may be used. The release is performed approximately 1 cm peripheral to the labrum. The anterior capsule is cut from the rotator interval to the inferior axillary pouch, sequentially releasing the middle and inferior (anterior band)
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B
C Figure 24-6. After full forward flexion is obtained, gentle external rotation is performed. A, The surgeon’s hands should be close to the glenohumeral joint to minimize the lever arm and risk of humeral fracture. Release allows full external rotation (B) and internal rotation (C).
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Figure 24-7. Arthroscopic view of a left shoulder from the posterior portal. The soft tissue structures of the rotator interval are excised, including the superior glenohumeral ligament and capsule. Note the biceps tendon running vertically along the right edge of the image.
Figure 24-9. Arthroscopic view of a left shoulder from the posterior portal toward the inferior axillary pouch. Inferior capsular release proceeds with care to avoid injury to the axillary nerve.
evaluation is performed, although only patients with preoperative impingement symptoms undergo decompression and bursectomy. Pearsall and associates24 have evaluated 46 patients who failed an average of 12 months of nonoperative management of adhesive capsulitis syndrome. They were treated with arthroscopic release of the involved shoulder. Release included the anteroinferior capsule, intra-articular portion of the subscapularis, middle glenohumeral ligament (MGHL), superior glenohumeral ligament (SGHL), and the coracohumeral ligaments. All 46 patients showed substantial gains in ROM and decreased pain.
Figure 24-8. Arthroscopic view of a left shoulder from the anterior portal. The posterior capsule is released using a combination of arthroscopic punches and electrocautery. The release is performed approximately 1 cm peripheral to the labrum. The infraspinatus and teres minor muscles are visible after capsular release.
glenohumeral ligaments. Inferior capsule release proceeds in the same fashion, with care taken inferiorly to avoid injury to the axillary nerve (Fig. 24-9). We prefer careful use of arthroscopic meniscal punches to complete the inferior release. Following release, a routine subacromial
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Postoperative care involves ROM exercises in a continuous passive ROM machine and passive- and active-assisted motion with a physical therapist. The interscalene catheter used during the surgical procedure is left in place postoperatively and the patient may be manipulated at the bedside the evening after surgery. We have found it helpful for the patient to visualize the motion gains early in the postoperative course while the regional anesthetic catheter is effective. A patient can be expected to remain hospitalized for 1 to 2 days. Physical therapy is done daily for the first 2 weeks after surgery.
Open Surgical Release Open surgical release has yielded mixed results and is not generally used as a treatment option for primary frozen shoulder. Morbidity is consistently higher in these patients when compared with those who have undergone
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arthroscopic releases. It is still indicated for some extraarticular causes for shoulder stiffness, such as malunion of the proximal humerus or glenoid. It does have the advantage of access to the entire humeroscapular motion interface and allows excision of heterotopic ossification and bone spurs, as necessary. For a contracted subscapularis muscle or tendon unit, open shoulder release allows the option of subscapularis musculotendinous lengthening. Ogilvie-Harris and colleagues25 have compared the results of arthroscopic capsular release with those of open surgical release for the treatment of frozen shoulder. Twenty patients were included in each group. At 2- to 5-year follow-up, both groups had similar shoulder motion. However, the arthroscopic release group had better functional recovery and less pain. At the first follow-up visit after surgical intervention, glenohumeral motion must be measured accurately. If the patient is unable to comply with the examination because of pain, an intra-articular xylocaine injection may be administered. Physical therapy is generally continued over the next 3 months. As the patient improves, a self-directed home stretching program is continued. If the patient experiences increased global stiffness, with no improvement in ROM, repeat MUA, arthroscopic release, or both is considered.
SUMMARY Adhesive capsulitis is a condition of global shoulder motion loss with limitation of active and passive glenohumeral motion resulting from contracture and loss of compliance of the glenohumeral joint capsule. Treatment depends on the stage of the disease process and functional demands of the patient with a ROM deficit. Early physical therapy and NSAIDs are helpful for relieving pain and increasing motion; however, resistant cases may require more aggressive treatment with manipulation under anesthesia or capsular release. A proper and well-designed rehabilitation program based on the stage of the patient is vital to a successful outcome. When physical therapy does not improve the patient’s condition, surgical intervention may be indicated. When appropriate, a controlled release may be obtained by manual manipulation or arthroscopic techniques; arthroscopic capsular release is now used as a primary modality for certain patients with resistant adhesive capsulitis. References 1. Codman EA: The Shoulder: Rupture of the Supraspinatus Tendon and Other Lesions in or About the Subacromial Bursa: Boston, Thomas Todd, 1934. 2. Neviaser JS: Adhesive capsulitis of the shoulder. J Bone Joint Surg 27: 211-222, 1945. 3. McKeever DC: Thawing the frozen shoulder: Clin Orthop 11:168-176, 1958.
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4. Neviaser JS: Adhesive capsulitis and the stiff and painful shoulder. Orthop Clin North Am 11:327-331, 1980. 5. Sheridan MA, Hannafin JA. Upper extremity: Emphasis on frozen shoulder: Orthop Clin North Am 37:531-539, 2006. 6. Smith SP, Devaraj VS, Bunker TD: The association between frozen shoulder and Dupuytren’s disease. J Shoulder Elbow Surg 10:149-151, 2001. 7. Massoud SN, Pearse EO, Levy O, Copeland SA: Operative management of the frozen shoulder in patients with diabetes. J Shoulder Elbow Surg 11:609-613, 2002. 8. Ogilvie-Harris DJ, Myerthall S: The diabetic frozen shoulder: Arthroscopic release. Arthroscopy 13:1-8, 1997. 9. Rodeo SA, Hannafin JA, Tom J, et al: Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder. J Orthop Res 15:427-436, 1997. 10. Bunker TD, Anthony PP: The pathology of frozen shoulder. A Dupuytren-like disease. J Bone Joint Surg Br 77:677-683, 1995. 11. Mengiardi B, Pfirrmann CW, Gerber C, et al: Frozen shoulder: MR arthrographic findings. Radiology 233:486-492, 2004. 12. Farrell CM, Sperling JW, Cofield RH: Manipulation for frozen shoulder: Long-term results. J Shoulder Elbow Surg 14:480-484, 2005. 13. Shaffer B, Tibone JE, Kerlan RK: Frozen shoulder. A long-term follow-up. J Bone Joint Surg Am 74:738-746, 1992. 14. Cyriax J: Textbook of Orthopaedic Medicine, vol 1. Diagnosis of Soft Tissue Lesions. 6th ed. London, Balliere Tindall, 1975, pp 76-77. 15. Light LE, Nuzik S, Personius W, et al: A low-load prolonged stretch vs high load in treating knee contractures. Phys Ther 64:330-334, 1984. 16. Warren CG, Lehmann JF, Kablanski JN: Elongation of rat tail tendon: Effect of load and temperature. Arch Phys Med Rehabil 52:465-474, 1971. 17. Warren CG, Lehmann JF, Kablanski JN: Heat and stretch procedures: An evaluation using rat tail tendon. Arch Phys Med Rehabil 57:122-126, 1976. 18. Tabarg JC, Tabarg C, Tardiev C: Physiological and structural changes in the cat’s soleus muscle caused by immobilization at different lengths by plaster casts. J Physiol 224:231-234, 1972. 19. Arem AJ, Madden JW: Effects of stress on healing wounds: Intermittent non-cyclical tension. J Surg Res 20:93-98, 1976. 20. McClure PW, Blackburn LG, Dusold C: The use of splints in the treatment of joint stiffness: Biologic rationale and an algorithm for making clinical decisions. Phys Ther 74: 1101-1107, 1994. 21. Lentell G, Hetherington T, Eagan J, et al: The use of thermal agents to influence the effectiveness of a low load prolonged stretch. J Orthop Sports Phys Ther 5:200-204, 1992. 22. Loew M, Heichel TO, Lehner B: Intra-articular lesions in primary frozen shoulder after manipulation under general anesthesia. J Shoulder Elbow Surg 14:16-21, 2005. 23. Andersen NH, Sojbjerg JO, Johannsen HV, Sneppen O: Frozen shoulder: Arthroscopy and manipulation under general anesthesia and early passive motion: J Shoulder Elbow Surg 7:218-222, 1998. 24. Pearsall AW 4th, Osbahr DC, Speer KP: An arthroscopic technique for treating patients with frozen shoulder. Arthroscopy 15:2-11, 1999. 25. Ogilvie-Harris DJ, Biggs DJ, Fitsialos DP, MacKay M: The resistant frozen shoulder. Manipulation versus arthroscopic release. Clin Orthop Relat Res (319):238-248, 1995.
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CHAPTER 25 Acromioclavicular
Joint Injuries Albert Tom, Augustus D. Mazzocca, and Christ J. Pavlatos
Acromioclavicular joint separation represents one of the most common shoulder injuries seen in general orthopedic practice. The most common mechanism of this injury is a fall with a direct force to the lateral aspect of the shoulder with the arm in an abducted position. Depending on the magnitude of injury to the acromioclavicular joint capsule and ligaments, as well as the coracoclavicular ligaments, these injuries can be classified with increasing severity as types I through VI. Typically, first- and second-degree sprains of the acromioclavicular joint, otherwise known as types I and II injuries, are treated conservatively, with the vast majority returning to preinjury status. Although the treatment of type III dislocations remain controversial, high-grade injuries, usually types IV to VI, with more than 100% in a posterior or inferior direction, or both, are typically treated surgically. This chapter will review the relevant anatomy, pathomechanics, examination, and treatment options for acromioclavicular joint injuries.
on the posteromedial side of the clavicle. The trapezoid ligament arises anteriorly and laterally to the conoid ligament on the coracoid process and extends to the undersurface of the clavicle, anterior and lateral to the conoid tubercle. The coracoclavicular ligaments play an important role in vertical stability. Studies by Fukuda and colleagues3 have shown that at large displacement, the conoid ligament provides the primary restraint to superior displacement. The trapezoid ligament is the primary restraint to acromioclavicular joint compression at small and large displacements.
ANATOMY
MECHANISMS OF INJURY
The acromioclavicular joint is classified as a diarthrodial joint and the articular surfaces are covered with fibrocartilage. There may be two types of fibrocartilaginous interarticular discs, complete and partial (meniscoid). There are great variations in size and shape. DePalma1 has shown that with age, the meniscus undergoes rapid degeneration until it is essentially no longer functional by the fourth decade. Nerve supply is from the branches of the axillary, suprascapular, and lateral pectoral nerves.
Most acromioclavicular injuries are caused by a direct fall on the point of the shoulder, with the arm at the side in the adducted position (Fig. 25-2). The downward force on the acromion results in a fracture of the clavicle. If no fracture occurs, the acromioclavicular ligaments are first stretched (mild sprain); then, as the force continues, the acromioclavicular ligaments tear and the coracoclavicular ligaments are stressed (moderate sprain). As the downward force continues, the coracoclavicular ligaments tear, along with the muscle attachments of the deltoid and trapezius muscles, resulting in a severe acromioclavicular sprain (complete dislocation).
According to Inman and associates,5 the clavicle rotates as the arm is elevated. There is a total range of motion of the acromioclavicular joint of 20 degrees, which occurs early (in the first 30 degrees of abduction) and late (after 135 degrees of elevation of the arm). During full elevation of the arm, the clavicle rotates about 40 degrees.
The acromioclavicular joint is inherently an unstable joint. It is stabilized by a set of ligaments and two muscles (Fig. 25-1). The first set are the acromioclavicular ligaments, which envelop the joint and are thick on the superior aspect and thin on the inferior aspect. Horizontal stability is controlled by the acromioclavicular ligaments.2 At small displacement, the acromioclavicular ligaments are the primary restraint to posterior and superior translation of the clavicle.3
CLASSIFICATION AND INCIDENCE Injuries to the acromioclavicular joint are best classified according to the amount of damage created by a given force. Allman categorized injuries to the acromioclavicular joint into grades I, II, and III.1 Rockwood and Young2 have identified six types, the first three of which are the same as Allman’s grades. Their additional types IV, V, and VI are Allman’s grade III injuries, varying only in the degree of direction of displacement of the distal part of the clavicle; the modified classification6 is as follows (Fig. 25-3).
The second set are the strong and heavy coracoclavicular ligaments, with fibers that run from the outer inferior surface of the clavicle to the base of the coracoid process of the scapula. These ligaments are divided into two parts.4 The conoid ligament is cone shaped, running from the posterior medial side of the coracoid to the conoid tubercle 303
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Lesser tuberosity
Type II Acromioclavicular joint disrupted, with tearing of acromioclavicular ligament Coracoclavicular ligament sprained Deltoid and trapezius muscles intact
Coracoid process
Bicipital groove
Figure 25-1. Normal anatomy of the acromioclavicular joint. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Type III Acromioclavicular ligament disrupted Acromioclavicular joint displaced; shoulder complex displaced inferiorly Coracoclavicular ligament disrupted, with coracoclavicular interspace 25% to 100% larger than normal shoulder Deltoid and trapezius muscles usually detach from distal end of clavicle
Type IV Acromioclavicular ligaments disrupted, acromioclavicular joint displaced, clavicle anatomically displaced posteriorly through trapezius muscle Coracoclavicular ligaments disrupted, with wider interspace Deltoid and trapezius muscles detached
Type V Acromioclavicular and coracoclavicular ligaments disrupted Acromioclavicular joint dislocated; gross displacement between clavicle and scapula (100% to 300% more than normal shoulder) Deltoid and trapezius muscles detached from distal end of clavicle
Type VI Acromioclavicular and coracoclavicular ligaments disrupted Distal clavicle inferior to acromion or coracoid process Deltoid and trapezius muscles detached from distal end of clavicle Figure 25-2. The most common mechanism of injury is a direct force that occurs from a fall on the point of the shoulder. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Type I Sprain of acromioclavicular ligament Acromioclavicular ligament intact Coracoclavicular ligament, deltoid and trapezius muscles intact
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Acromioclavicular (AC) dislocations account for 12% of all dislocations about the shoulder.2 Injuries are more common in male than female patients, with a ratio of 5:1 to 10:1. Incomplete injuries to the acromioclavicular joint are twice as common as complete dislocations.
DIAGNOSIS The pain associated with AC injury may be difficult to localize because of the complex sensory innervation of the joint. A history revealing an acute injury, as described earlier, is
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Normal
Type I
Type IV
Type II
Type V
Conjoined tendon of biceps and coracobrachialis Type III
Type VI
an important starting point in the diagnosis. The lack of a discrete injury with AC joint pain and joint separation is instead consistent with a degenerative condition. Given an acute injury, it is important to determine the level of perceived pain and its location, as well as any history of previous shoulder injuries. During examination, the patient should be upright so that the weight of the arm will help exaggerate any deformities.
Figure 25-3. Schematic representations of the classification of ligamentous injuries that can occur to the acromioclavicular ligament. Type I, A mild force applied to the point of the shoulder does not disrupt the acromioclavicular or coracoclavicular ligaments. Type II, A moderate to heavy force applied to the point of the shoulder will disrupt the acromioclavicular ligaments, but the coracoclavicular ligaments remain intact. Type III, When a severe force is applied to the point of the shoulder, the acromioclavicular and coracoclavicular ligaments are disrupted. Type IV, In this major injury, not only are the acromioclavicular and coracoclavicular ligaments disrupted, but the distal end of the clavicle is displaced posteriorly into or through the trapezius muscle. Type V, A violent force has been applied to the point of the shoulder that not only ruptures the acromioclavicular and coracoclavicular ligaments but also disrupts the deltoid and trapezius muscle attachments and creates a major separation between the clavicle and acromion. Type VI, Another major injury is an inferior dislocation of the distal end of the clavicle to the subcoracoid position. The acromioclavicular and coracoclavicular ligaments are disrupted. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
extremity is depressed when compared with the normal shoulder. Patients with type IV dislocations often present with significant pain, with a prominence noted on the posterior aspect of the shoulder. When viewed from above and
Pain and swelling are the most common symptoms seen in injuries to the AC joints. Mild to moderate pain is noted in types I and II AC joint injuries, respectively. Swelling, although minimal in type I AC joint sprains, is more prominent in type II AC joint injuries, making palpation of the slightly prominent clavicle difficult. In type III AC joint injuries, significant pain and swelling are noted, with a noticeable prominence of the distal clavicle. Gross displacement of the distal end of the clavicle and tenting of the skin are seen in type V AC joint injuries (Fig. 25-4). The patient characteristically presents with the upper extremity adducted close to the body and held upward by the other arm to relieve the discomfort in the affected joint. The entire upper
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A
B
Figure 25-4. Type V acromioclavicular dislocations. A, The clavicle is quite prominent, secondary to the downward displacement of the right upper extremity. B, Severe prominence of the right clavicle. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, vol 1. Philadelphia, WB Saunders, 1990, p 427.)
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behind the patient, the distal end of the clavicle may be seen displaced through the fibers of the trapezius muscle.
RADIOGRAPHIC EVALUATION Radiographic evaluation of the AC joint will clearly demonstrate any displacement of the distal clavicle. Standard radiographs should include anteroposterior and lateral views of the AC joint.2 Standard anteroposterior views (Fig. 25-5) are taken with a 10- to 15-degree cephalic tilt (Fig. 25-6) to avoid superimposition of the AC joint on the spine of the scapula.7 Upward displacement of the clavicle, as well as increased distance between the undersurface of the clavicle and the coracoid process, will confirm AC dislocations. Posterior dislocations may be missed on standard anteroposterior views. A scapular lateral view, as described by Alexander,8 will help identify posterior dislocations. Patients in whom it is difficult to differentiate type II from type III AC joint injuries may require stress films of both shoulders. These stress films will test the integrity of the coracoclavicular ligaments and assist in evaluating the degree of displacement of the distal end of the clavicle. These films are taken with the patient sitting or standing and 10 to 15 pounds of weight suspended from each wrist. Anteroposterior views of both shoulders are taken. A difference of 25% in the distance from the coracoid process to the clavicle in the injured and normal shoulders will confirm a complete AC dislocation.
A
B
TREATMENT The management of injuries to the AC joint may range from benign neglect to the use of slings,9 braces,10 harnesses,11 or several surgical procedures, as described in the literature.12-20 Most clinicians agree on conservative or nonoperative management of acute types I and II AC sprains. The treatment of acute type III AC joint dislocations is controversial. There are three basic and fundamental different views concerning the management of acute type III AC joint dislocations: 1. Nonoperative or conservative approach 2. Surgical repair recommended for all patients 3. Surgical repair recommended for select patients
C Figure 25-5. Why the acromioclavicular joint is poorly visualized on routine shoulder radiographs. A, This routine anteroposterior view of the shoulder shows the glenohumeral joint well. However, the acromioclavicular joint is too dark to interpret, because that area of the anatomy has been overpenetrated by the x-ray technique. B, When the exposure usually used to take the shoulder films is decreased by two thirds, the acromioclavicular joint is well visualized. However, the inferior corner of the acromioclavicular joint is superimposed on the acromion process. C, Tilting the tube 15 degrees upward provides a clear view of the acromioclavicular joint. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Management of Specific Injuries Type I The type I injury involves a mild sprain of the AC ligaments, with the AC and coracoclavicular ligaments intact. Treatment consists of application of ice bags to relieve discomfort and a sling to support the extremity for several days. Active-assisted range of motion is initiated immediately, followed by isometric strengthening. Once full
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motion and strength have returned, the patient may return to normal activities. Type II The type II injury involves disruption of the AC ligament, with the coracoclavicular ligament intact. Most clinicians agree that nonsurgical measures are indicated to treat this
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X-ray
10°
Figure 25-8. Plaster cast device for acromioclavicular separations (older method used in 1952). (From Rowe CR: Acromioclavicular and sternoclavicular joints. In Rowe CR (ed): The Shoulder. New York, Churchill Livingstone, 1988, p 293.)
Figure 25-6. Position of the patient for Zanca view using 10- to 15-degree cephalic tilt of the standard view for the acromioclavicular joint. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, vol 1. Philadelphia, WB Saunders, 1990, p 427.)
injury. However, there are differences of opinion as to which conservative measure is indicated. Many use a sling9 for 7 to 14 days to rest the shoulder, followed by a gradual rehabilitation program. Others have recommended the use of adhesive tape strappings,21 harnesses,10 and a plaster cast.22 Allman23 has recommended the use of a sling harness immobilizing device, the Kenny-Howard sling (Fig. 25-7), for 3 weeks. Some have recommended a plaster cast device (Fig. 25-8), as described by Urist,22 with a strap over the top of the clavicle in an effort to depress the clav-
Figure 25-7. Kenny-Howard shoulder halter for acromioclavicular separations. (From Rowe CR: Acromioclavicular and sternoclavicular joints. In Rowe CR (ed): The Shoulder. New York, Churchill Livingstone, 1988, p 293.)
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icle down to the acromion. However, the problem is a depressed upper extremity and not an elevated clavicle. These harnesses and devices can be used for 3 to 6 weeks to prevent another injury from converting a type II subluxation to a type III dislocation. Heavy lifting and contact sports should be avoided for approximately 8 to 12 weeks, until the ligaments have completely healed. Although conservative management has been recommended for types I and II injuries, reports from Bergfeld and coworkers24 and Cox25 have suggested that these injuries may cause more problems than previously recognized. In type I injuries, 36% of patients have residual symptoms, with radiographic changes in 70%. In type II injuries, 48% to 65% of patients have symptoms, with radiographic changes in 75%. These injuries may require excision of the outer 2 cm of the clavicle, as described by Mumford.26 This can be performed via an open or arthroscopic technique with gratifying results. In athletes, the Mumford procedure has produced successful results, as reported by Cook and Tibone.27 Twenty-three athletes were followed for an average of 3.7 years after a Mumford procedure for type I or II AC joint injuries. Most of the athletes achieved preinjury performance levels after the procedure, with little weakness noted with slow-speed and no weakness noted with high-speed isokinetic testing. Type III The management of type III AC injuries has created much controversy in the orthopedic literature. Many have recommended the nonoperative approach.9,28-36 Most agree that a simple sling is adequate for rest and comfort. As in type II injuries, a gradual rehabilitation program begins as symptoms subside over a 7- to 14-day period. The use of a harness to reduce the dislocation has not been as rewarding. The harness must be worn continuously for 6 weeks to maintain a reduction, but few patients can comply with this form of management.
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This conservative approach has become more popular during the past 10 years, because the patient loses little time from work or athletics and does not have to be hospitalized. Cox25 has reported improved results with no support to the arm in 62% of patients, whereas with immobilization and a sling only 25% improved at 3 to 6 weeks. Further studies have also recommended conservative treatment of type III AC injuries. Glick and associates32 have reported on 35 unreduced type III AC dislocations in athletes. They concluded that a complete reduction is unnecessary and that none of the athletes were disabled at follow-up. Bjerneld,29 Dias,30 and Sleeswijk and colleagues,36 and Schwarz and Leixnering,35 have also reported on a series of patients with type III AC injuries treated nonoperatively, with 90% to 100% satisfying results and with follow-ups averaging 5 to 7 years. Studies comparing operative and nonoperative treatments of type III have also supported conservative measures. In their comparative studies, Hawkins9 and Bannister,28 Galpin,31 Imatani,33 Larsen34 and associates have concluded that nonoperative treatment yields good, if not better, results than surgical treatment. Operative management of complete type III AC dislocations may be indicated for patient populations such as laborers, throwers, or other athletes. Types IV, V, and VI Because of the severe posterior displacement in type IV injuries and gross displacement in type V injuries, most clinicians have recommended a surgical repair.37-41 Few type VI injuries have been described in the literature42-45; all were treated with surgery. Attempts at closed reduction are usually unsuccessful. Gerber and Rockwood42 have reported using the extra-articular technique with a coracoclavicular lag screw, repair of the ligaments, and imbrication of the deltoid trapezius fascia over the top of the clavicle, with successful results. The rehabilitation following surgery to correct a type IV, V, or VI sprain tends to be somewhat slower because of the severity of the initial injury. The program is similar to those discussed and matches the exact surgical procedure and specific patient demands and desires.
Recommended Technique The literature is replete with surgical techniques to address complete AC dislocations, including primary repair of the coracoclavicular ligaments, augmentation with autogenous tissue (coracoacromial ligament), augmentation with absorbable and nonabsorbable sutures and prosthetic material, including coracoclavicular stabilization with metallic screws.37-41,46-75 The Weaver-Dunn technique using transfer of the coracoacromial ligament has been the most popular procedure for acute and chronic injuries. Several
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more recent reports have described good results with modifications of the Weaver-Dunn technique. Anatomic Coracoclavicular Reconstruction From a biomechanical perspective, the importance of the coracoclavicular and AC ligaments in controlling superior and horizontal translations has been elucidated. Failure to reproduce conoid, trapezoid, and AC ligament function surgically with current techniques may explain the observed incidence of recurrent instability and pain. We advocate using a separate, more robust graft source to improve surgical results. The use of a free autogenous or allograft tendons have been further supported in the biomechanics laboratory. Box 25-1 lists some recommendations when performing procedures. BOX 25-1.
Surgical Pearls
• Include the entire clavicle to the SC joint in the operative field for draping to allow for wide exposure. • Place a small towel bump under the medial scapular edge. • Bullet the semitendinosus ends to allow for easy graft passage. • Make sure that the head of the patient can be repositioned to the side to allow room for conoid tunnel drilling. • Instead of repositioning the patient’s head, an alternative is to displace the clavicle anteriorly with a towel clip to allow access for conoid tunnel drilling. • Make a skin incision over the coracoid process, more medially than usual (not over the AC joint). • Make a medial skin incision to allow direct visualization of the coracoclavicular ligament and coracoid. • Tag the deltoid and trapezial fascia for good repair. • Pass sutures under the coracoid from medial to lateral or lateral to medial. • If passing lateral to medial, make sure that the medial coracoid base is exposed and insert a Darrach retractor on the medial base to catch the suture-passing device. • Do not spin the reamer out to avoid tunnel widening. • Over-reduce the AC joint if the distal clavicle is resected; abut the clavicle to the coracoid process. • Do not over-reduce the clavicle if the distal clavicle is to be preserved. • Insert 5.5- ⫻ 8-mm Peek screws into the 5.5-mm bone tunnel (line to line). • Drill up to 1⁄2 mm if the graft is too big for screw fixation. • Insert the Peek screw anterior to the graft to re-create the posterior coracoclavicular ligaments equally.
SC, sternoclavicular.
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Procedure Anesthesia and Positioning. The patient is placed in the beach chair position after induction of general anesthesia. Ensure that the head is mobile for possible repositioning. A small bump is placed on the medial scapular edge to elevate the coracoid anteriorly. Drape wide to expose the sternoclavicular (SC) joint and posterior clavicle. The arm is free-draped. Exposure. A no. 10 scalpel is used to make a 6-cm longitudinal incision, centered over or slightly medial to the coracoid. Medial and lateral skin flaps are elevated with a needle-tipped bougie. Gelpi retractors are used to assist with exposure. A transverse incision is made along the midaxis of the clavicle, extending into the AC joint. Full-thickness flaps of the superior AC joint capsule are elevated superiorly and inferiorly with a needle-tipped bougie. The anterior and posterior portion of the distal clavicle is completely exposed (Fig. 25-9). Five mm of distal clavicle is resected if AC joint arthrosis is present. The medial and lateral coracoid base is exposed with a Cobb elevator. A headlight may be useful for this portion of the procedure. Care is taken to avoid excessive medial dissection to prevent musculocutaneus nerve injury.
Figure 25-10. Distal clavicle resection.
The standard of care is to perform a distal clavicle resection (Figs. 25-10 and 25-11). However, there is tremendous variability in the AC joint and there seems to be tremendous stability from an intact AC joint. Therefore, we believe that it may be advantageous to preserve the distal clavicle and we have done this in select patients. Passing Under the Coracoid. A specially designed cannulated suture-passing device (Arthrex, Naples, Fla) is passed medially to laterally around the coracoid. A FiberWire or FiberStick (Arthrex) is then shuttled through the cannulated handle and retrieved laterally at the tip. This passing stitch is later used for graft passage around the coracoid (Figs. 25-12 and 25-13).
Figure 25-11. Beveling posterior edge of distal clavicle.
An alternate means of coracoid graft fixation is biotenodesis screw fixation of the looped end of the semitendinosus
Figure 25-12. FiberWire placed around coracoid.
graft in a coracoid base bone tunnel. This is best achieved by positioning the 7-mm offset AC ligament guide on the medial coracoid base and reaming an 8- to 9-mm bone tunnel.
Figure 25-9. Initial surgical exposure.
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Clavicular Tunnels. The conoid ligament tunnel is established with a guide pin drilled 4.5 cm medially from the
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Figure 25-13. Close-up of FiberWire around coracoid.
Figure 25-15. Placing guide pins in tunnels.
intact lateral distal clavicle edge. This is positioned along the posterosuperior cortex and marked before distal clavicle resection. The pin is directed 30 degrees anteriorly, aiming toward the coracoid. A second guide pin from the Arthrex biotenodesis set is drilled in the center of the clavicular anteroposterior (AP) dimension, 1.5 cm lateral to the medial pin. This tunnel will be used to reconstruct the trapezoid ligament and is again directed 30 degrees anteriorly toward the coracoid (Figs. 25-14, 25-15, and 25-16). A 5.5-mm reamer is used to ream both tunnels (Figs. 25-17 and 25-18). The reamer is removed by hand twisting after penetrating the far cortex to avoid tunnel widening. Graft Preparation. An allograft semitendinosus graft is contoured to fit through a 5.5-mm tunnel. A no. 2 FiberWire is used to place baseball stitches at each end of the graft (Fig. 25-19).
Figure 25-16. Measuring guide pins.
Graft Passage. The initially passed FiberWire or FiberStick is used to shuttle the prepared semitendinosus graft along with an additional no. 2 FiberWire around the coracoid process. The accessory FiberWire will provide secondary fixation. The free ends of the semitendinosus graft along
Figure 25-17. Reaming conoid tunnel.
with the free no. 2 FiberWire is shuttled into the respective clavicular bone tunnels using a Hewson suture passer (Fig. 25-20).
Figure 25-14. Marking clavicular tunnels.
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Biotenodesis Fixation. A 5.5- ⫻ 8-mm PEEK tenodesis screw is then loaded onto the Bio-Tenodesis screwdriver
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will also help reduce the clavicle. If the distal clavicle is preserved, we avoid over-reducing the AC joint. A second PEEK tenodesis screw is inserted into the second clavicular tunnel through the FiberWire suture. The graft is tensioned as the screw is inserted. The actual order of tunnel fixation is unimportant. The FiberWire is then tensioned and tied with surgeon knots. The graft ends are then sutured to one another and the excess graft is excised.
Figure 25-18. Reaming trapezoid tunnel.
Superior Acromioclavicular Joint Capsular Ligament Repair. No. 2 FiberWire stitches are used to imbricate the superior AC joint capsular ligaments in a pants-over-vest configuration. This will offer additional AP stability to the reconstruction. The deltoid trapezius fascia is also repaired in this step as full thickness flaps of fascia and AC joint capsular ligaments are elevated in a single layer. Closure. After copious wound irrigation, 2-0 Vicryl sutures are used to close the subcutaneous tissues. A 3-0 Monocryl suture is used to perform a subcutaneous skin closure. The wound is injected with bupivacaine (Marcaine). Follow-up. Sutures are removed after approximately the first 7 days. Patients are typically seen at 1, 2, 3, and 6 months and then annually (Fig. 25-21) for examination. During these visits, postoperative x-rays include bilateral Zanca views to measure the coracoid’s clavicular distances.
Figure 25-19. Preparing graft.
REHABILITATION The patient is instructed to wear a sling for the first 8 weeks. Postoperative rehabilitation begins with gentle exercises for the patient, including immediate pendulum exercises and passive external rotation to 30 degrees.
Figure 25-20. Graft passage.
(Arthrex). The nitinol loop retriever is used to pass the FiberWire through the cannulated screwdriver system. With countertension on the opposite graft end, the PEEK screw is inserted flush to the cortical surface. The clavicle is then over-reduced with downward pressure from a Cobb elevator. A superiorly directed force on the humerus
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Figure 25-21. Postoperative x-ray obtained during re-examination of patient.
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These exercises are progressed to include active range of motion at week 8 and isotonic strengthening at 12 to 16 weeks. Sports-specific activities and return to full athletics usually occur between weeks 16 and 24. Heavy laborers may return to work activities at approximately 6 months postoperatively.
SUMMARY On review of the literature, types I and II acromioclavicular joint injuries are best treated conservatively, with good results seen in most patients. A certain percentage of these patients may have residual pain and stiffness as a result of degenerative changes, which may necessitate excision of the distal clavicle in some patients. In both types of injury, immediate motion and strengthening appear to yield better success. Results of treatment of type III acromioclavicular joint injuries have been successful in nonoperative and operative groups. Based on these findings, a nonoperative approach to this injury would be appropriate for most patients. If pain is noted on follow-up, an operative procedure may be performed. Types IV, V, and VI injuries are best treated with open reduction and surgical stabilization of the acromioclavicular joint.
References 1. DePalma AF: The role of the disks of the sternoclavicular and acromioclavicular joints. Clin Orthop 13:7, 1959. 2. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Rockwood CA, Matsen FA III (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 413. 3. Fukuda K, Craig EV, An K-N et al: Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 68:434, 1986. 4. Johnston TB, Davies DV, Davies F (eds): Gray’s Anatomy, 32nd ed. London, Longmans, Green, 1958. 5. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg Am 26:1, 1944. 6. Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP (eds): Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, pp 860. 7. Zanca P: Shoulder pain: Involvement of the acromioclavicular joint: Analysis of 1,000 cases. AJR Am J Roentgenol 112:493, 1971. 8. Alexander OM: Dislocation of the acromio-clavicular joint. Radiography 15:260, 1949. 9. Hawkins RJ: The acromioclavicular joint. Presented at the American Academy of Orthopaedic Surgeons Summer Institute, Chicago, July 10-11, 1980. 10. Giannestras NJ: A method of immobilization of acute acromioclavicular separation. J Bone Joint Surg Am 26:597, 1944. 11. Warner AH: A harness for use in the treatment of acromioclavicular separation. J Bone Joint Surg Am 19:1132, 1937.
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12. Augereau B, Robert H, Apoil A: Treatment of severe acromioclavicular dislocation: A coracoclavicular ligamentoplasty technique derived from Cadenat’s procedure. Ann Chir 35:720, 1981. 13. Bateman JE: Athletic injuries about the shoulder in throwing and body-contact sports. Clin Orthop 23:75, 1962. 14. Bearden JM, Hughston JC, Whatley GS: Acromioclavicular dislocation: Method of treatment. J Sports Med 1:5, 1973. 15. Bosworth BM: Acromioclavicular separation: New method of repair. Surg Gynecol Obstet 73:866, 1941. 16. Bundens WD Jr, Cook JI: Repair of acromioclavicular separations by deltoid-trapezius imbrication. Clin Orthop 20:109, 1961. 17. Dewar FP, Barrington TW: The treatment of chronic acromioclavicular dislocation. J Bone Joint Surg Br 47:32, 1965. 18. Sage FP, Salvatore JE: Injuries of acromioclavicular joint: Study of results in 96 patients. South Med J 56:486, 1963. 19. Weaver JK, Dunn HK: Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg Am 54:1187, 1972. 20. Weitzman G: Treatment of acute acromioclavicular joint dislocation by a modified Bosworth method: Report on twenty-four cases. J Bone Joint Surg Am 49:1167, 1967. 21. Rawlings G: Acromioclavicular dislocations and fractures of the clavicle. A simple method of support. Lancet 2:789, 1939. 22. Urist MR: Complete dislocation of the acromioclavicular joint: The nature of the traumatic lesion and effective methods of treatment with an analysis of 41 cases. J Bone Joint Surg Am 28:813, 1946. 23. Allman FL Jr: Fractures and ligamentous injuries of the clavicle and its articulation. J Bone Joint Surg Am 49:774, 1967. 24. Bergfeld JA, Andrish JT, Clancy WG: Evaluation of the acromioclavicular joint following first- and second-degree sprains. Am J Sports Med 6:153, 1978. 25. Cox JS: The fate of the acromioclavicular joint in athletic injuries. Am J Sports Med 9:50, 1981. 26. Mumford E: Acromioclavicular dislocation. J Bone Joint Surg Am 23:799, 1941. 27. Cook FF, Tibone JE: The Mumford procedure in athletes: An objective analysis of function. Am J Sports Med 16:97, 1988. 28. Bannister GC, Wallace WA, Stableforth PG, Hutson M: The management of acute acromioclavicular dislocation. J Bone Joint Surg Br 71:848, 1989. 29. Bjerneld H, Hovelius L, Thorling J: Acromio-clavicular separations treated conservatively: A 5-year follow-up study. Acta Orthop Scand 54:743, 1983 30. Dias JJ, Steingold RA, Richardson RA et al: The conservative treatment of acromioclavicular dislocation: Review after five years. J Bone Joint Surg Br 69:719, 1987. 31. Galpin RD, Hawkins RJ, Grainger RW: A comparative analysis of operative versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop 193:150, 1985. 32. Glick JM, Milburn LJ, Haggerty JF, Nishimoto D: Disclocated acromioclavicular joint: Follow-up study of 35 unreduced acromioclavicular dislocations. Am J Sports Med 5:264, 1977. 33. Imatani RJ, Hanlon JJ, Cady GW: Acute complete acromioclavicular separation. J Bone Joint Surg Am 57:328, 1975. 34. Larsen E, Bjerg-Neilsen A, Christensen P: Conservative or surgical treatment of acromioclavicular dislocation: A prospective, controlled, randomized study. J Bone Joint Surg Am 68:552, 1986.
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35. Schwarz N, Leixnering M: Results of nonreduced acromioclavicular Tossy III separations. Unfallchirurg 89:248, 1986. 36. Sleeswijk-Visser SV, Haarsma SM, Speeckaert MT Conservative treatment of acromioclavicular dislocation: Jones strap versus mitella [abstract]. Acta Orthop Scand 55:483, 1984. 37. Barber F: Complete posterior acromioclavicular dislocation: A case report. Orthopedics 10:493, 1987. 38. Hastings DE, Horne JG: Anterior dislocation of the acromioclavicular joint. Injury 10:285, 1978. 39. Malcapi C, Grassi G, Oretti D: Posterior dislocation of the acromioclavicular joint: A rare or an easily overlooked lesion? Ital J Orthop Traumatol 4:79, 1978. 40. Nieminen S, Aho AJ: Anterior dislocation of the acromioclavicular joint. Ann Chir Gynaecol 73:21, 1984. 41. Sondergard-Petersen P, Mikkelsen P: Posterior acromioclavicular dislocation. J Bone Joint Surg Br 64:52, 1982. 42. Gerber C, Rockwood CA Jr: Subcoracoid dislocation of the lateral end of the clavicle: A report of three cases. J Bone Joint Surg Am 69:924, 1987. 43. McPhee I: Inferior dislocation of the outer end of the clavicle. J Trauma 20:709, 1980. 44. Patterson WR: Inferior dislocation of the distal end of the clavicle. J Bone Joint Surg Am 49:1184, 1967. 45. Sage J: Recurrent inferior dislocation of the clavicle at the acromioclavicular joint. Am J Sports Med 10:145, 1982. 46. Grauthoff VH, Klammer HL: Complications because of migration of a Kirschner wire from the clavicle. Fortschr Rontgenstr 128:591, 1978. 47. Mazet RJ: Migration of a Kirschner wire from the shoulder region into the lung: Report of two cases. J Bone Joint Surg Am 25:477, 1943. 48. Norrell H, Llewellyn RC: Migration of a threaded Steinmann pin from an acromioclavicular joint into the spinal canal: A case report. J Bone Joint Surg Am 47:1024, 1965. 49. Rockwood CA Jr, Green DP (eds): Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984. 50. Kennedy JC, Cameron H: Complete dislocation of the acromioclavicular joint. J Bone Joint Surg Br 36:202, 1954. 51. Kennedy JC: Complete dislocation of the acromioclavicular joint: 14 years later. J Trauma 8:311, 1968. 52. Lowe GP, Fogarty MJP: Acute acromioclavicular joint dislocation: Results of operative treatment with the Bosworth screw. Aust N Z J Surg 47:664, 1977. 53. Alldredge RH: Surgical treatment of acromioclavicular dislocation. Clin Orthop 63:262, 1969. 54. Kappakas GS, McMaster JH: Repair of acromioclavicular separation using a Dacron prosthesis graft. Clin Orthop 131:247, 1978. 55. Park JP, Arnold JA, Coker TP, et al: Treatment of acromioclavicular separations: A retrospective study. Am J Sports Med 8:251, 1980. 56. Tagliabue D, Riva: Current approaches to the treatment of acromioclavicular joint separation in athletes. Ital J Sports Traumatol 3:15, 1981. 57. Dahl E: Velour prosthesis in fractures and dislocations in the clavicular region. Chirurgerie 53:120, 1982.
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58. Bargren JH, Erlanger S, Dick HM: Biomechanics and comparison of two operative methods of treatment of complete acromioclavicular separation. Clin Orthop 130:267, 1962. 59. Kiefer H, Claes L, Burri C, Holzworth J: The stabilizing effect of various implants on the torn acromioclavicular joint: A biomechanical study. Arch Orthop Trauma Surg 106:42, 1986. 60. Lancaster S, Horowitz M, Alonso J: Complete acromioclavicular separations: A comparison of operative methods. Clin Orthop 216:80, 1987. 61. Taft TN, Wilson FC, Oglesby JW: Dislocation of the acromioclavicular joint: An end-result study. J Bone Joint Surg Am 69:1045, 1987. 62. Rauschning W, Nordesjo LO, Nordgren B et al: Resection arthroplasty for repair of complete acromioclavicular separations. Arch Orthop Traumatol Surg 97:161, 1980. 63. Smith DW: Coracoid fracture associated with acromioclavicular dislocation. Clin Orthop 108:165, 1975. 64. Smith MJ, Stewart MJ: Acute acromioclavicular separations. Am J Sport Med 7:62, 1979. 65. Bailey RW, O’Connor GA, Tilus PD, Baril JD: A dynamic repair for acute and chronic injuries of the acromioclavicular area [abstract]. J Bone Joint Surg Am 54:1802, 1972. 66. Bailey RW: A dynamic repair for complete acromioclavicular joint dislocation [abstract]. J Bone Joint Surg Am 47:858, 1965. 67. Berson BL, Gilbert MS, Green S: Acromioclavicular dislocations: Treatment by transfer of the conjoined tendon and distal end of the coracoid process to the clavicle. Clin Orthop 135:157, 1978. 68. Caspi I, Ezra E, Neurbay J, Horoszovski H: Musculocutaneous nerve injury following dynamic fixature of distal clavicle. Clin Orthop 1985. 69. Costic RS, Labriola JE, Rodosky ME, Debski RE: Biomechanical rationale for development of anatomical reconstruction of coracoclavicular ligaments after complete acromioclavicular joint dislocations. Am J Sports Med 32:1929, 2004. 70. Lee SJ, Nicholas SJ, Akizuki KH, et al: Reconstruction of the coracoclavicular ligaments with tendon grafts. Am J Sports Med 31:648, 2003. 71. Grutter PW, Petersen S: Anatomical acromioclavicular ligament reconstruction. Am J Sports Med 31:1, 2005. 72. Mazzocca AD, Santangelo SA, Johnson ST, et al: A biomechanical evaluation of an anatomical coracoclavicular ligament reconstruction. Am J Sports Med 34:236, 2006. 73. Jari R, Costic RS, Rodosky MW, Debski RE: Biomechanical function of surgical procedures for acromioclavicular joint dislocations. Arthroscopy 20:237, 2004. 74. Jones HP, Lemos MJ, Schepsis A: Salvage of failed acromioclavicular joint reconstruction using autogenous semitendinosus tendon from the knee. Am J Sports Med 29:234,2001. 75. Debski RE, Parson IM, Woo S, Fu FH: Effect of capsular injury on acromioclavicular joint mechanics. J Bone Joint Surg Am 83:1344, 2001.
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CHAPTER 26 Shoulder Arthroplasty
in the Athletic Shoulder Todd S. Ellenbecker and David S. Bailie
The most common reasons and diagnostic classifications for which shoulder arthroplasty is performed are degenerative osteoarthritis, secondary degenerative osteoarthritis, capsulorrhaphy arthropathy, and rheumatoid arthritis.1 Although all four of these can be found in the athletic shoulder, degenerative osteoarthritis occurring solely from repetitive overuse and wear or secondary to athletic trauma, as well as capsulorrhaphy arthropathy, are particularly common indications in the athlete. A brief overview of each diagnostic classification has implications for the role of shoulder arthroplasty in the treatment of arthritis in the athletic shoulder.
Characteristic wear of the subchondral bone and glenoid cartilage in the shoulder with degenerative osteoarthritis occurs posteriorly, often leaving an area of intact cartilage anteriorly.5 The cartilage of the humeral head is typically eroded in a pattern of central baldness, the so-called Friar Tuck pattern (Fig. 26-1). This differs from the pattern of humeral head wear in cuff tear arthropathy, in which a chronic large rotator cuff defect subjects the uncovered humeral head to abrasion against the acromion and coracoacromial arch, resulting in superior rather than central wear patterns. Recent research by Mochizuki and colleagues6 has identified specific patterns of glenoid load distribution in the throwing shoulder at the anterior, anteroinferior, posterior, and posteroinferior aspects of the dominant glenoid. These were compared with more central glenoid load patterns in the contralateral shoulder and in the shoulder of nonthrowing subjects. The repetitive loading of the athletic shoulder is further compromised in cases of glenohumeral instability.6,7
DEGENERATIVE GLENOHUMERAL OSTEOARTHRITIS Degenerative osteoarthritis of the glenohumeral joint is less common than in the weight-bearing joints (e.g.,. hip, knee) of the lower extremity, accounting for only 3% of all osteoarthritis lesions.2 Osteoarthritis of the glenohumeral joint (GHOA) can be classified as primary or secondary. Primary GHOA usually manifests with no apparent antecedent cause, whereas secondary GHOA results from a preexisting problem, such as a previous fracture, avascular necrosis, burned out rheumatoid arthritis, or crystalline arthropathy.
Another important diagnosis for which shoulder arthroplasty is performed is capsulorrhaphy arthropathy.1 In 1982, Neer and associates8 initially reported glenohumeral arthritis after anterior shoulder instability in an initial series of 26 patients with prior anterior or posterior instability who underwent shoulder arthroplasty. Many patients in this series had prior stabilization surgery. Samilson and Prieto9 later suggested the term dislocation arthropathy in their study of 74 patients with glenohumeral arthritis with prior anterior and posterior instability.
Athletes at risk include weightlifters, throwing athletes (baseball players, softball players) and those engaged in racquet sports (tennis, racquetball, squash).3 This degenerative osteoarthritis seems to be the end result of trauma, whether from pure instability, repetitive loading, fracture, rotator cuff arthropathy, or postsurgery. At the macroscopic level of osteoarthritis (OA), cartilage is noted to have irregularity, with delamination of the cartilage surface and eventually frank cartilage loss, resulting in bone on bone contact in the joint. Early in the degenerative process, inflammatory cells are seen, but this effect is transient and inflammation is not considered to play a major long-term role. Biochemically, OA is associated with a decrease in glycosaminoglycan (GAG) levels, including chondroitin sulfate and hyaluronic acid, increased water content because of increased permeability of water diffusing into the cartilage as GAGs are lost, and increased enzymatic activity from metalloproteinases (MMPs). MMPs play an important role in degeneration of the extracellular matrix of cartilage.4
Neer10 has further reported on the association of osteoarthritis and glenohumeral instability by finding subluxation of the humerus in the direction opposite that of the initial instability caused by excessive tightening at the time of initial stabilization surgery. Matsen and coworkers11 have coined the term capsulorrhaphy arthropathy for patients who develop OA as a consequence of overly tightened soft tissue structures in the treatment of glenohumeral joint instability. Buscayret and colleagues12 have reported the incidence of glenohumeral osteoarthritis to range between 12% and 62% following operative treatment of shoulder instability. Factors specific to stabilization procedures that may contribute to the development of glenohumeral arthritis include encroachment on the articular cartilage by hardware, laterally placed bone block in a Bristow or Latarjet procedure, and excessive soft tissue tensioning resulting from a Putti-Platt procedure.13
Wear patterns in the human shoulder vary based on the types of underlying arthritic condition and causative factors. 315
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Tight anterior capsule
P
External rotation
Obligate posterior translation Figure 26-1. Central pattern of humeral head cartilage wear (Friar Tuck pattern).
Figure 26-2. Concept of obligate translation. P, posterior directed translation.
CONCEPT OF OBLIGATE TRANSLATION
rotator cuff tissue, stability, activity level and desire, and age. Hettrich and coworkers18 have studied preoperative factors in 71 shoulders from 68 patients who underwent shoulder hemiarthroplasty to determine which factors contributed to greater postoperative success. Patients with a preoperative absence of glenoid erosion, no previous surgery, and intact rotator cuff showed significantly greater improvement in active range of motion, more postoperative comfort, and ability to lift weight above shoulder level than patients with glenoid erosion, prior surgery, or rotator cuff tears.
The concept of obligate translation has been applied extensively in orthopedic and sports physical therapy, and in orthopedics in general, since the publication of the study by Harryman and colleagues.14 They identified increases in anterior humeral head translation and shear following a controlled posterior capsular placation in cadaveric specimens. Obligate translation, defined as the translation of the humeral head in the direction opposite that of the tight capsule and soft tissue structures, has been a paramount concept applied in the treatment of the overhead athlete with subtle anterior glenohumeral joint instability secondary to adaptive posterior rotator cuff and posterior capsule tightness.15,16 Harryman and associates17 have also reported the presence of obligate translation in flexion, internal and external rotation, and maximal elevation with shoulder arthroplasty following insertion of an oversized humeral head prosthesis. Shoulder arthroplasty can tend to cause global capsular restriction because of the substitution of a humeral head prosthesis for a degenerative and collapsed humeral head. This overstuffing can prohibit return of optimal range of motion unless the patient undergoes adequate capsular release and early postoperative physical therapy to address capsular tightness.5 Figure 26-2 demonstrates the concept of obligate translation.
INDICATIONS Patients who do not respond to nonoperative therapy and have a progressive loss of range of motion and strength are candidates for shoulder arthroplasty. Shoulder arthroplasty and hemiarthroplasty can provide symptomatic relief and restoration of function in individuals with glenohumeral arthritis. The type of surgical procedure chosen is dependent on overall shoulder function, anatomy, condition of bone and
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Indications for humeral hemiarthroplasty are primary glenohumeral osteoarthritis, secondary degenerative joint disease, osteonecrosis of the humeral head, and combined loss of glenohumeral joint surface and rotator cuff.18 Hemiarthroplasty remains an attractive option for younger patients because of concerns about the longevity of the glenoid prosthesis. Additionally, cementless surface replacement arthroplasty replaces only the damaged portion of the joint-bearing surface, with the advantages of minimal bone resection and restoration of normal anatomy, including humeral head version, inclination, and offset without a humeral stem.19
Surgical Considerations Athletes represent a unique subset of patients with shoulder arthritis that may require arthroplasty. The goals must be to restore full motion and strength and preserve the anatomy for potential revision in the future. One must also consider the types of sports involved (collision versus noncollision) and dominance of the extremity. Conservative measures, such as nonsteroidal antiinflammatory drugs (NSAIDs), steroid injections (occasional), hyaluronic acid preparations (e.g., viscosupplementation), physical therapy to increase motion and restore strength, and arthroscopic débridement, must have failed before considering arthroplasty in the athletic population.
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Optimizing rotator cuff status with arthroscopic subacromial decompression, repair of rotator cuff tears, or both may precede the arthroplasty or be done concurrently. The selected implant should provide immediate stability to limit micromotion with therapy and sports and be durable, revisable, and allow for anatomic reconstruction. The need to replace the glenoid may dictate overall postoperative ability to participation in sports, because this is still the weak link in shoulder arthroplasty. Placement of a glenoid component entails the risk of early loosening with more physical activities. Performing a more anatomic reconstruction theoretically may reduce the incidence of radiographic and real glenoid loosening by limiting eccentric loading of the component. Restoring the anatomy will also ensure optimal kinematics to maximize motion, strength, and recovery potential. In general, surgical considerations must first include anatomic joint reconstruction with a well-fixed stable implant. This is done with a humeral head resurfacing implant or a third- or fourth-generation stemmed implant. The ultimate goal is to match the native humeral version, inclination, offset, and height. The glenoid can then be resurfaced with a prosthesis or managed with a number of nonimplant resurfacing techniques. Finally, the soft tissues must be released, balanced, and repaired to allow for adequate restoration of long-term function. Although every surgeon may have a preference, we use resurfacing primarily for those patients who desire to return to high-demand activities, such as strength training, collision sports (e.g., skiing, football, mountain biking), tennis, basketball, and martial arts.20 We also have chosen to avoid placing a glenoid component in these individuals to avoid the potential pitfalls of loosening and revision. Other alternatives we have used include microfracture, reaming the glenoid to restore version, and bone grafting cysts and defects with biologic covering of the glenoid surface with autograft or allograft tissue. Key to the success of arthroplasty in any patient, but especially in those who desire to return to more demanding sports, is restoration of soft tissue tension. Specifically, a complete 360-degree subscapularis release is needed to increase excursion and restore external rotation. Lengthening the tendon is not needed and will ultimately weaken this structure, with the potential for delayed rupture. This release will allow the humeral head to return to the center of the glenoid and permit the normal obligate translation that occurs with rotational motion. This in turn helps restore the normal forces across the glenohumeral joint and leads to decreased pain, improved strength, and function (Figs. 26-3, 26-4, and 26-5). Rehabilitation considerations must take into account the amount of motion obtained under anesthesia after subscapularis closure. This should be communicated to the patient and therapist. The goal is to obtain normal motion, which can be achieved in almost all cases. The subscapularis
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Figure 26-3. Shoulder arthroplasty. Intra-operative photo of a severely arthritic humeral head in a young patient, resulting in poor function and pain.
Figure 26-4. Shoulder arthroplasty. Subscapularis closure after shoulder arthroplasty. The repair must be protected post-operatively, while attempting to regain motion of the shoulder in rehabilitation.
repair must be sound and protected for the first 6 weeks; external rotation is limited to 30 to 45 degrees. If a larger rotator cuff repair is performed, these precautions should also be instituted according to the surgeon’s confidence in the repair. Full passive range of motion (ROM) can be obtained immediately, with rapid progression to activeassisted and active ROM during the initial 6 weeks. Communication with the therapist is critical; we encourage preoperative evaluation to meet the specific needs and desires of the patient after surgery.
REHABILITATION The surgical exposure used during shoulder arthroplasty has significant ramifications for the immediate postoperative management of these patients. Two approaches are typically used—the deltopectoral approach and anterosuperior or
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TABLE 26-1 Factors Affecting Progression of Rehabilitation Following Arthroplasty
Figure 26-5. X-ray of shoulder arthroplasty. Radiograph of a cementless humeral resurfacing arthroplasty in a young patient with a history of glenohumeral arthrosis.
Mackenzie approach.21 The skin incision for the anterosuperior approach extends distally in a straight line from the acromioclavicular (AC) joint for a distance of 9 cm. The anterior deltoid fibers are split for a distance of not more than 6 cm to protect the axillary nerve. The acromial attachment of the deltoid is detached to expose the anterior aspect of the acromion. The subscapularis is completely released and held by stay sutures and detached. The long head of the biceps can be dislocated posteriorly over the humeral head as the humeral head is dislocated anteriorly.19,21 The complete release and detachment of the subscapularis with this approach are required to gain exposure for preparation of the humeral head during hemiarthroplasty, as well as during total shoulder arthroplasty (Table 26-1).
Subscapularis Precautions For the first 6 weeks, specific subscapularis precautions must be followed to protect this important structure postoperatively. This entails limitation of passive or active external rotation ROM and no active resistive exercise for internal rotation. Although gentle attempts at passive external rotation can occur to as far as 30 to 45 degrees of external rotation beyond neutral, techniques that place increased or undue tension on the anterior capsule and subscapularis are avoided for the first 6 weeks following surgery. Additional precautions may be needed, depending on the repair of additional rotator cuff tendons at the time of surgery, as well as whether bicep tenolysis, tenodesis, or tenotomy has been performed. Specifically,
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Factor
Indication
Subscapularis release and repair—exercise in first 6 weeks postoperatively
Limitation of external rotation ROM and resistive internal rotation
Supraspinatus tear and repair—elevation, delayed active abduction range of motion (ROM)
Delayed reattainment of antigravity
Biceps tenolysis and tenodesis—6 weeks postoperatively
No resistive elbow flexion exercise in initial 6 weeks postoperatively
Age, tissue quality
Delayed return of active ROM
resistive exercise for the biceps brachii is not performed for the first 6 weeks postoperatively if a release of the biceps long head or tenodesis has been performed to minimize the chance of rerupture and reappearance of a Popeye deformity. It is beyond the scope of this chapter to discuss the entire rehabilitation process following shoulder arthroplasty; a detailed summary of our postoperative protocol is presented in Box 26-1.
Range of Motion and Optimization of Capsular Relationships Concomitant with therapy during the initial stages of postoperative rehabilitation are the use of mobilization and passive stretching to decrease abnormal glenohumeral joint shear forces14,15 and improve gross glenohumeral joint ROM. Typical patterns of ROM loss following shoulder injury adhere to the predictable pattern described by Cyriax and Cyriax,22 which states that external rotation, abduction, and internal rotation are most limited, followed by forward flexion, which is least limited.22 To address selective capsular tightness, posterior glides of the humeral head relative to the glenoid, with varying degrees of internal rotation of the glenohumeral joint, are used to mobilize the posterior capsule and address limitations in internal glenohumeral joint rotation. Anterior glides of the humeral head are often used later in the rehabilitation process once initial subscapularis healing has occurred to address limitations in external rotation, if indicated. Optimization of capsular length between the anterior and posterior capsule is theoretically purported to minimize humeral head shear within the glenoid with glenohumeral joint movement.14,15 In addition to the use of glenohumeral joint mobilization, application of passive stretching using the low-load, long-duration stretching concept is also recommended.23
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BOX 26-1.
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Rehabilitation Following Glenohumeral Joint Arthroplasty
General Guidelines
glenohumeral joint in scapular plane and 10-20 degrees of abduction (towel roll or pillow under axilla)
• Sling use and duration as directed by surgeon in postoperative instructions • Immediate postoperative passive and active-assisted range of motion (ROM) consisting of stomach rubs, sawing movements, and elbow range of motion as instructed following hospital discharge
Postoperative Weeks 6-8
Postoperative Weeks 1-4
2. Initiation of internal rotation submaximal resistive exercise progression
1. Modalities to decrease pain and inflammation 2. Passive range of motion initiated, with no limitation in flexion, abduction, or internal rotation; no external rotation stretching or anterior capsular mobilization in this rehabilitation phase to protect subscapularis repair; movement-ROM into 30-40 degrees external rotation with 30-45 degrees abduction allowed by therapist, provided it is not against tension 3. Elbow, wrist, and forearm ROM and stretching 4. Manually applied scapular resistive exercise for protraction and retraction, submaximal biceps and triceps manual resistance with shoulder in supported position supine 5. Ball approximation (closed-chain Codman’s exercise) using Swiss ball or tabletop
Postoperative Weeks 2-4
1. Initiation of passive external rotation ROM and stretching beyond neutral rotation position
3. Traditional rotator cuff isotonic exercise program a. Side-lying external rotation b. Prone extension c. Prone horizontal abduction—limited from neutral to scapular plane position initially, with progression to coronal plane as ROM improves 4. Biceps and triceps curls in standing position, with glenohumeral joint in neutral resting position 5. Oscillation exercise with resistance bar or Bodyblade (Hymanson, Marina Del Rey, Calif) 6. Rhythmic stabilization in open and closed kinetic chain environments
Postoperative Weeks 8-12 1. Continuation of resistive exercise and ROM progressions
1. Initiation of active-assisted ROM using pulley for sagittal plane flexion and scapular plane elevation
2. Addition of ball dribbling and upper body plyometrics with small Swiss ball
Postoperative Weeks 4-6
Postoperative Weeks 12-24
1. Continuation of above program
1. Continuation of rehabilitation
2. Initiation of submaximal multiple-angle isometrics and manual resistive exercises for shoulder external rotation, abduction and adduction, flexion and extension
2. Isometric internal and external rotation strength testing and assessment in neutral scapular plane position
3. Upper body ergometer (UBE)
3. Subjective rating scale completion
4. External rotation isotonic exercises using pulley, weights, or tubing, with elbow supported and
4. ROM assessment
Strengthening Early strengthening following glenohumeral arthroplasty focuses on the scapular stabilizers and safe, submaximal rotator cuff activation.16,24 Techniques described in Chapter 50 show manual scapular stabilization for retraction and protraction. This allows for early contraction of the lower trapezius and serratus anterior force couple components without stressing the glenohumeral joint. Multiple sets to induce muscular fatigue of these important muscles are indicated.16 In addition to the scapular stabilization exercise, early application of external rotation exercise is initiated. As noted,
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internal rotation strengthening cannot commence before 6 weeks postoperatively to protect the subscapularis muscle tendon unit. Progression of rotator cuff strengthening follows patterns outlined in the literature, with documented high levels of activation of the posterior rotator cuff to enhance recruitment and improve local muscular endurance with multiple sets of 15 to 20 repetitions.25-28 Additional application of resistive exercise and proprioceptive training occurs in the supine position; the patient places the shoulder in 90 degrees of shoulder flexion with assistance from the therapist. This position is termed the balance point position because patients can balance the extremity in this position despite being unable to elevate the shoulder to 90 degrees
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independently. From this position, the therapist can progressively apply manual contacts or modified rhythmic stabilization while the patient provides cocontraction to maintain this position. Additionally, in this early stage, external rotation isometrics with elastic resistance using a TheraBand (Hygenic, Akron, Ohio) are performed (Fig. 26-6). The neutral position is used, with a towel roll placed under the axilla. This is maintained during the exercise and the patient steps laterally away from the attachment point of the tubing. After a several-second pause at the point of increased tension, the patient is directed to step back toward the attachment point of the tubing again. Actual motion at the glenohumeral joint does not occur but variable loading during this isometric exercise is transmitted to the glenohumeral and scapulothoracic muscles. This exercise is well tolerated and safe, and can be used as a home exercise program to facilitate development of the posterior rotator cuff and scapular stabilizers.
Rotator Cuff and Scapular Exercise Progression Gradual progressions in rotator cuff and scapular strengthening occur with increased intensity and variety following 5 to 6 weeks postoperatively. The important role of the
rotator cuff musculotendinous units in controlling and centering the humeral head, especially during midrange movement patterns, cannot be underestimated.29 Submaximal strengthening methods to recruit the rotator cuff musculature selectively, using exercise patterns that place the shoulder in neutral nonimpinging positions, forms the basis for in-clinic and home-based rehabilitative exercise programs. Exercises such as side-lying external rotation, prone extension, and prone horizontal abduction are used and recommended, based on electromyographic research studies that documented high levels of posterior rotator cuff activation.25-28 As a general rule, shoulder exercises that keep the shoulder below 90 degrees of elevation and the arm slightly anterior to and in the scapular plane are recommended.16 Progressive advances in exercise for the muscles that stabilize the scapula are also indicated. Exercises that strengthen the serratus anterior and lower trapezius are particularly recommended to improve scapular upward rotation during elevation.30 Resistance patterns with light weights, medicine balls, or a Thera-Band can be used to perform shoulder punches, with emphasis on the position of maximal scapular protraction (termed the plus position) to recruit the serratus anterior.31,32 Scapular retraction exercises, such as rowing with multiple positions of arm abduction, are also indicated. Lower resistance levels allow rotator cuff activation, with less compensation and shoulder girdle elevation that often accompany independent exercise programs with higher resistance levels and movement patterns characterized by full, end-range, overhead elevation. Care must be taken to ensure that resistive exercise does not elevate pain levels, which lead to muscular inhibition and compensation. The restoration of optimal muscle balance is imperative during the rehabilitation of all shoulder injuries and pathologies, but it is particularly important following shoulder arthroplasty. Figures 26-7 and 26-8 illustrate the effect of unbalanced muscular forces during shoulder muscular contraction and volitional movement. Unbalanced internal rotation strength or dominant anterior muscular strength development can lead to anterior translation of the humeral head relative to the glenoid.29 Similarly, excessive posterior development can accentuate posterior subluxation from an eroded posterior glenoid and overly tight anterior structures (obligate translation) and produce posterior instability.
Figure 26-6. Dynamic isometric step-outs. This exercise uses elastic resistance, with the patient holding the arm in neutral rotation with a towel roll or bolster under the involved arm. Holding the arm in this position, the subject repeatedly takes a large step away from the attachment site of the tubing while holding the extremity stationary. A step back to the starting position completes one repetition of this exercise.
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Optimal muscle balance between the external and internal rotators has been reported and recommended in the range from 66% to 75% external rotation (ER) to internal rotation (IR).33,34 This can be assessed with a hand-held dynamometer or isometric function of an isokinetic dynamometer system to ensure proper restoration of this optimal muscle balance.33,35 Patients frequently present with overly dominant anterior muscular strength, which can
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321
Unbalanced net force Applied force
Balanced net force Applied force
Figure 26-7. Diagrammatic representation of unbalanced muscular force.
jeopardize glenohumeral mechanics and lead to complications and functional impairment. The rocking horse phenomenon (see Fig. 26-8) can lead to implant loosening, one of the most frequently encountered complications following total shoulder arthroplasty.5,11 Restoration of proper muscular balance via monitoring and addressing the ER/IR strength ratio, as well as application of ROM, physiologic stretching, and accessory mobilization techniques during postoperative rehabilitation, ensure proper capsular excursion and minimize the effects of obligate translation. Research studies14,15,36 have shown the effects of capsular tightness on glenohumeral kinematics. Progression to elevated positions of rotator cuff and scapular stabilization is indicated to assist patients with the return of shoulder elevation against gravity following these extensive surgical procedures. Figure 26-9 shows an exercise position using the scapular plane, 80 to 90 degrees of elevation, and an exercise ball. The patient is asked to maintain his or her position on the ball while the therapist provides challenges or perturbations to the extremity in all
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Figure 26-8. Rocking horse phenomenon. Loosening of the glenoid component results when translation of the head on the glenoid produces eccentric forces on the glenoid component. (From Matsen FA III, Lippitt SB, Sidles JA, and Harryman DT II. Practical evaluation and management of the shoulder. Philadelphia, WB Saunders, 1994.)
directions to elicit muscular activation in this functional position. As with all shoulder elevation exercises, great care is taken to avoid the presence of excessive scapular elevation, which results in the shoulder hiking during exercise.37 This compensatory pattern leads to the development of inappropriate motor patterns and produces long-term scapular pathology with arm elevation. The exercises listed in this chapter minimize positions and movement patterns that increase glenohumeral contact forces and compressive loading.38 The use of closed kinetic chain exercise in the
Figure 26-9. Closed-chain scapular plane exercise using exercise ball on the wall (exercise ball from Hygenic, Akron, Ohio.)
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form of weightbearing is minimized in the initial postoperative rehabilitation exercise progression.38,39
OUTCOMES Following arthroplasty, careful monitoring of the patient for ROM and muscular strength enables the progression of mobilization and stretching using objectively based guidelines to be monitored. We have determined ROM, strength, and functional rating scores 12 weeks following total arthroplasty (PROMOS stemmed implant, Promos Shoulder System, Smith-Nephew Orthopaedics, Memphis, TN) and hemiarthroplasty (Copeland shoulder, Biomet, Warsaw, Ind) when the patient is still typically under the care of a physical therapist in a supervised rehabilitation program.38 Our results show average antigravity flexion and abduction ROM to be approximately 135 degrees, 70 degrees of external rotation with 90 degrees of abduction, and 35 degrees of internal rotation with 90 degrees of glenohumeral joint abduction. Muscular strength measured isometrically using a dynamometer revealed a 47% deficit in external rotation strength compared with the contralateral extremity and a 35% deficit in internal rotation strength. The self-report section of the Modified ASES rating scale produced values of 31 of 45 points in these patients following total and hemiarthroplasty, with comparable values of 38 of 45 points in patients following mini-open rotator cuff repair in the same 12-week postoperative time frame. Longer term follow-up has been done following hemiarthroplasty and total shoulder arthroplasty, although limited data are available on younger, more athletic patient populations at present. Levy and Copeland19 have reported on long-term results (more than 2 years; mean, 7.6 years) following Copeland cementless humeral resurfacing (Biomet, Warsaw, Ind) in 42 elderly patients. Constant scores improved from 20 points preoperatively to 61.9 points postoperatively at final follow-up. Of particular importance was the improvement of active elevation from a mean of only 59.9 degrees preoperatively to 128 degrees postoperatively for those undergoing total shoulder replacement and 124 degrees postoperatively for those undergoing hemiarthroplasty. Of these patients, 89.9% considered their shoulder much better or better following the procedure.
final follow-up. Similar increases in active external rotation were reported, ranging from 4 to 38 degrees. Results were reported as good or excellent in 50 of 55 patients. Further research is clearly needed to establish the short- and longterm outcomes of patients following hemiarthroplasty and total shoulder arthroplasty, particularly in the younger, active athletic patient. The American Shoulder and Elbow Surgeons Society has recommended guidelines for return to sports activity following shoulder arthroplasty (Table 26-2). Current research continues to identify osteoarthritic changes in the overhead athlete.40,41 Maquirrain and associates41 have reported a 33% incidence of osteoarthritic changes in older tennis players (mean age, 57.2 years). The incidence of glenohumeral arthritic changes was higher in this study than in age-matched sedentary control subjects. Additional research on specific populations of overhead athletes will likely identify early degenerative changes in the shoulder that may ultimately require shoulder arthroplasty.
SUMMARY The combination of high-load activity and repetitive overuse can lead to osteoarthritic changes in the athletic shoulder. Early recognition and treatment of the arthritic shoulder in the athlete, coupled with advances in humeral and glenoid components, have allowed patients to return to higher levels of function following shoulder arthroplasty. TABLE 26-2 Activity Recommendations After Total Shoulder Arthroplasty
Recommended
Allowed With Experience Not Recommended
Bicycling
Golf
Football
Swimming
Ice skating
Hockey
Cross-country skiing Shooting
Gymnastics
Speed walking
Rock climbing
Downhill skiing
Jogging Doubles tennis Low-impact aerobics Bowling
Matsoukis and colleagues13 have evaluated 55 patients who had suffered a prior dislocation 45 months following shoulder arthroplasty. The mean delay between the instability event and arthroplasty was 24.2 years, with an average age of 55.9 years; 24 patients had undergone a prior stabilization procedure to address their instability, including coracoid transfers and Putti-Platt–type soft tissue transfer procedures. Constant scores improved from 30.8 preoperatively to a mean of 65.8 at follow-up. Active forward elevation improved from 82 degrees preoperatively to 138 degrees at
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Canoeing Croquet Shuffleboard Horseshoes Ballroom dancing *Based on 1999 American Shoulder and Elbow Surgeons Society recommendations. From Healy WL, Iorio R, Lemos MJ: Athletic activity after joint replacement. Am J Sports Med 29:377-388, 2001.
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The rehabilitation guidelines discussed have included the protection of anterior structures during initial range-ofmotion and progressive resistive exercises for the return of rotator cuff and scapular strength. These are keys for successful rehabilitation programs for these patients. Further advances in orthopedic technology and research, including biologic resurfacing42 and microfracture, may lead to additional options for the younger active patient with glenohumeral arthritis. More basic science and patient outcomes research studies are needed to develop optimal patient management techniques for glenohumeral arthritis in the athletic shoulder. References 1. Parsons M, Campbell B, Titelman RM, et al: Characterizing the effect of diagnosis on presenting deficits and outcomes after total shoulder arthroplasty. J Shoulder Elbow Surg 14:575-584, 2005. 2. Badet R, Boileau P, Noel E, Walch G: Arthrography and computed arthrotomography study of seventy patients with primary glenohumeral osteoarthritis. Rev Rhum Engl Ed 62:555-562, 1995. 3. Andrews J: Arthroscopic débridement for glenohumeral arthritis. Presented at the Symposium of the American Orthopaedic Society for Sports Medicine (AOSSM): Arthritis of the Glenohumeral Joint in the Young Patient. March 2000. 4. Carfagno DC, Ellenbecker TS: Osteoarthritis of the glenohumeral joint: Nonsurgical treatment options. Physician Sports Med 30:19-32, 2002. 5. Rockwood CA, Wirth MA, Lippitt SB: Glenohumeral arthritis and its management. In Rockwood CA, Matsen FA III (eds): The Shoulder. Philadephia, WB Saunders, 1998, pp 840-964. 6. Mochizuki Y, Natsu K, Kashiwagi K, et al: Changes of the mineralization pattern in the subchondral bone plate of the glenoid cavity in the shoulder joints of the throwing athletes. J Shoulder Elbow Surg 14:616-619, 2005. 7. Schultz CU, Anetzberger H, Pfahler M, et al: Anterior shoulder instability modifies glenoid subchondral bone density. Clin Orthop Relat Res (423):259-263, 2004. 8. Neer CS, Watson KC, Stanton FJ: Recent experience in total shoulder replacement. J Bone Joint Surgery Am 64:319-337, 1982. 9. Samilson RL, Prieto V: Dislocation arthropathy of the shoulder. J Bone Joint SurgeryAm 65:456-460, 1995. 10. Neer CS: Shoulder Reconstruction. Philadelphia, WB Saunders, 1990, pp 208-212 . 11. Matsen FA, Rockwood CA, Wirth MA, Lippitt SB: Glenohumeral arthritis and its management. In Rockwood CA, Matsen FA III (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 1998, pp 879-888. 12. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment. Am J Sports Med 32:1165-1172, 2004. 13. Matsoukis J, Tabib W, Guiffault P, et al: Shoulder arthroplasty in patients with a prior anterior shoulder dislocation. J Bone Joint Surgery Am 85:1417-1423, 2003. 14. Harryman DT, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990.
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15. Grossman MG, Tibone JE, McGarry MH, et al: A cadaveric model of the throwing shoulder: A possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am 87:824-831, 2005. 16. Ellenbecker TS: Nonoperative Treatment of the Shoulder. New York, Thieme, 2006. 17. Harryman DT, Sidles JA, Harris SL, et al: The effect of articular conformity and the size of the humeral head component on laxity and motion after glenohumeral arthroplasty. A study in cadavera. J Bone Joint Surg Am 77:555-563, 1995. 18. Hettrich CM, Weldon E, Boorman RS, et al: Preoperative factors associated with improvements in shoulder function after humeral hemiarthroplasty. J Bone Joint Surgery Am 86:1446-1451, 2004. 19. Levy O, Copeland SA: Cementless surface replacement arthroplasty (Copeland CSRA) for osteoarthritis of the shoulder. J Shoulder Elbow Surgery 13:266-270, 2004. 20. Bailie DS, Ellenbecker TS: Shoulder arthroplasty in patients under 55 years of age. Abstract AAOS-2006. 21. Levy O, Funk L, Sforza G, Copeland SA: Copeland surface replacement arthroplasty of the shoulder in rheumatoid arthritis. J Bone Joint Surgery Am 86:512-518, 2004. 22. Cyriax, JH, Cyriax PJ: Illustrated Manual of Orthopaedic Medicine. London, Butterworths, 1983. 23. Bonutti PM, Windau JE, Ables BA, Miller BG: Static progressive stretch to reestablish elbow range of motion. Clin Orthop Relat Res (303):128-134, 1994. 24. Wilcox RB, Arslanian LE, Millett P: Rehabilitation following total shoulder arthroplasty. J Orthop Sports Phys Ther 35:821-836, 2005. 25. Ballantyne BT, O’Hare SJ, Paschall JL, et al: Electromyographic activity of selected shoulder muscles in commonly used therapeutic exercises. Phys Ther 73:668-677, 1993. 26. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis of posterior rotator cuff exercises. Athletic Training 25:40-45, 1990. 27. Reinhold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34:385-394, 2004. 28. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. 29. Lee SB, An KN: Dynamic glenohumeral stability provided by three heads of the deltoid muscle. Clin Orthop Rel Research (400):40-47, 2002. 30. Kilber WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998. 31. Mosely JB, Jobe FW, Pink M: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 32. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. 33. Davies GJ: A Compendium of Isokinetics in Clinical Usage. LaCrosse, Wisc, S & S Publishing, 1984. 34. Ivey FM, Calhoun JH, Rusche K, Bierschenk J: Isokinetic testing of shoulder strength: Normal values. Arch Phys Med Rehabil 66:384-386, 1985. 35. Ellenbecker TS, Davies GJ: The application of isokinetics in testing and rehabilitation of the shoulder complex. J Athletic Training 35:338-350, 2000.
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36. Koffler KM, Bader D, Eager M, et al: The effect of posterior capsular tightness on glenohumeral translation in the late-cocking phase of pitching: A cadaveric study [abstract SS-15]. Presented at the Arthroscopy Association of North America Annual Meeting, Washington, DC, April 2001. 37. Kibler WB, Uhl TL, Maddux JWQ, et al: Qualitative clinical evaluation of scapular dysfunction: A reliability study. J Shoulder Elbow Surgery 11:550-556, 2002. 38. Conzen A, Eckstein F: Quantitative determination of articular pressure in the human shoulder joint. J Shoulder Elbow Surgery 9:196-204, 2000. 39. Ellenbecker TS, Davies GD: Closed Kinetic Chain Exercise: A Comprehensive Guide to Multiple-Joint Exercise. Champaign, Ill, Human Kinetics, 2001.
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40. Ellenbecker TS, Sum J, Bailie DS: Glenohumeral joint range of motion, rotational muscle strength and functional self-report following shoulder arthroplasty. J Orthop Sports Phys Ther 36:28, 2006. 41. Maquirrain J, Ghisi P, Amato, S: Is tennis a predisposing factor for degenerative shoulder disease? A controlled study in former elite players. Br J Sports Med 40:447-450, 2006. 42. Krishnan, SG, Burkhead, WZ, Nowinski RJ: Humeral hemiarthroplasty with biologic resurfacing of the glenoid and acromion for rotator cuff tear arthropathy. Tech Shoulder Elbow Surg 5:51-59, 2004.
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CHAPTER 27 Neurovascular Compression
Syndromes of the Shoulder Champ L. Baker, Jr. and Champ L. Baker III
During athletic activities, tremendous shear and compressive loads are placed on the glenohumeral joint and supporting structures. Repetitive overhead activities place the athlete’s shoulder at risk. Common problems caused by these activities in the overhead athlete include labral injury, joint instability, impingement, and rotator cuff failure. However, neurovascular compression syndromes, such as thoracic outlet syndrome, axillary artery occlusion, effort thrombosis, and quadrilateral space syndrome, should be considered in the differential diagnosis. Although they are less common, these entities should be considered during the examination of the injured athlete. The signs and symptoms of neurovascular compression are often vague and can be frequently overlooked. Diagnosis and treatment are commonly delayed. Failure of prompt recognition and treatment of neurovascular compression syndromes of the shoulder can lead to progressive dysfunction and disability.
occluded by external pressure exerted by the pectoralis minor muscle when the arm is brought overhead. Peet and associates,15 in 1956, were the first to use the term thoracic outlet syndrome. Brantigan and Roos16 have defined the syndrome as upper extremity neurovascular symptoms presumably caused by narrowing of the thoracic outlet through which the major vessels and nerves pass.
NEUROVASCULAR COMPRESSION SYNDROMES Thoracic Outlet Syndrome Thoracic outlet syndrome is an ill-defined term that encompasses the signs and symptoms attributed to compression of the neurovascular structures as they traverse the space from the neck to the axilla. Because of the intimate proximity of the nerves and vessels to each other in this space, varying degrees of compression of the brachial plexus and subclavian vessels can exist. Thus, the clinical presentation of this syndrome can be highly variable. Although Wood and coworkers17 have stated that this complex syndrome is “incompletely understood, difficult to diagnose, and often poorly managed,” a thorough understanding of the anatomy is essential for the clinician treating an athlete with this disorder.
HISTORY The earliest reports of neurovascular compression in the shoulder focused on thoracic outlet syndromes. In 1743, Hunald (cited by Tyson and Kaplan1) was the first to describe cervical ribs as an anatomic anomaly causing thoracic outlet compression. Coote,2 in 1861, performed a successful decompression of the thoracic outlet by surgically removing the offending cervical rib. Similarly, Murphy3 in 1905 and Keen4 in 1907 reported the symptoms of neurovascular compression and the role of the cervical rib. Stopford and Telford5 in 1919 and Wheeler6 in 1920 showed that thoracic outlet structures could be compressed by the first thoracic rib and that surgical removal of the rib alleviated associated symptoms. Brickner and Milch,7 in 1925, suggested strengthening the shoulder girdle suspensory muscles in patients with thoracic outlet compression but without a cervical rib. Adson and Coffey8 were the first to describe successful relief of thoracic outlet compression by sectioning the scalenus anticus muscle in their 1927 report. Their results were confirmed in similar reports by Ochsner and colleagues9 in 1935 and Naffziger and Grant10 in 1938. Costoclavicular level neurovascular compression secondary to hyperabduction of the arm was first described by Lewis and Pickering11 in 1934 and later by Eden in 1939.12 Vascular compression in this region was defined as costoclavicular syndrome by Falconer and Weddel13 in 1943. Wright,14 in 1945, reported on a hyperabduction syndrome in which the second part of the axillary artery is
The thoracic outlet is the space extending from the supraclavicular fossa to the axilla; it includes the costoclavicular space, which is the interval between the clavicle and first rib. The anterior primary rami of the C5-T1 nerves exit their respective intervertebral foramen to form the brachial plexus as they pass through the anterior and middle scalene muscles (Fig. 27-1). The anterior scalene muscle originates from the transverse processes of the third through sixth cervical vertebrae and inserts posterior to the subclavian vein onto the first rib. The middle scalene muscle originates from the transverse processes of the second through seventh cervical vertebrae and inserts behind the subclavian artery into the first rib. The subclavian artery joins the trunks of the brachial plexus lying on the anterior aspect of the middle scalene muscle. Thus, the brachial plexus and subclavian artery travel through a triangle bordered by the middle scalene muscle laterally and the anterior scalene muscle medially, with the first rib as the base.18 The subclavian vein courses anterior to the anterior scalene muscle as it passes over the first rib, before joining the subclavian artery and brachial 325
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C3 C4
C6 Cervical rib C7
Anterior scalene muscle Middle scalene muscle Posterior scalene muscle Brachial plexus
C5
C6
Fibrous bands
T1
Subclavian artery C7 T1
Figure 27-2. Fibrous bands originating from a cervical rib. Figure 27-1. Thoracic outlet anatomy.
plexus as they pass through the costoclavicular space and continue beneath the coracoid process, posterior to the pectoralis minor muscle. Although there is considerable controversy regarding the exact pathophysiology of thoracic outlet syndrome, there are several basic concepts. Symptomatic compression of the neurovascular structures results from a mechanical space problem of the thoracic outlet. One theory states that afflicted patients have one or more congenital anomalies that predispose them to developing symptoms. Any superimposed trauma or insult can narrow the available space further and cause compression from muscle swelling, hemorrhage, or fibrosis.19 Such congenital anomalies include cervical ribs, fibrous bands, and scalene muscle abnormalities (Fig. 27-2). A well-developed cervical rib is the most common bony abnormality associated with thoracic outlet syndrome.20 It has been found in approximately 0.5% to 1% of the general population, with approximately 50% of patients demonstrating bilaterality.21 Several clinicians have noted compression in patients in the absence of cervical ribs and have determined the presence of congenital fibrous bands connecting an elongated cervical transverse process or adventitial rib to the first rib as an important causative factor.22-25 Compression of the brachial plexus can result from abnormalities of the first rib. Roos22 has described nine different types of congenital bands that could produce compression in the thoracic outlet. Swank and Simon23 have described variations in the insertion of the scalene muscles on the first rib, and others have targeted the anterior scalene muscle as the ultimate culprit.24,25 Another theory in the pathogenesis of thoracic outlet syndrome proposes that conditions that increase the
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descent of the scapula further bring the neurovascular structures downward and can result in compression.18 Injury to the neck or trapezius and other supporting structures, with later weakness or disuse atrophy, could increase the descent of the scapula and result in symptoms.26,27 Other aggravating factors include obesity and poor posture. Lastly, the costoclavicular space can be narrowed from exuberant callus formation from a clavicular nonunion or malunion,28,29 an anomalous subclavius muscle,30 or pulling the shoulders down and back as if in a military brace position. The clinical presentation of thoracic outlet syndrome is highly variable, depending on which neurovascular structures at risk are compressed—neurologic, arterial, or venous. Thus, there are no pathognomonic signs or symptoms to confirm this syndrome, and it is often a diagnosis of exclusion.31 The disorder is most commonly found in women. Thoracic outlet syndrome has been reported in baseball players, rowers,32 swimmers,33,34 wrestlers,35 football players,36 and long distance runners.37 Many patients report an episode of trauma preceding the onset of symptoms.19,31,38,39 Although the subjective complaints can vary secondary to the compromised thoracic outlet structures, up to 98% of patients report some neurologic symptoms.19 In a study of 236 patients with a diagnosis of thoracic outlet syndrome who later underwent transaxillary first rib resection, paresthesia of the hand was the most common complaint, present in 90% of patients, with the little finger affected four times as often as the thumb.38 Most patients identify symptoms in the ulnar nerve or lower trunk distribution. Pain can be present in the hand, forearm, arm, neck, chest, and head. Because of intrinsic muscle involvement, weakness of grip strength and loss of manual dexterity may be noticeable. An athlete may
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also complain of fatigue, weakness, or heaviness of the upper extremity. Significant vascular compression can result in swelling, cyanosis, coldness, pallor, and fatigue or claudication-type symptoms with exercise. Leffert and Perlmutter,38 in 1999, reported overhead activities as being provocative in 89% of patients, and symptoms could usually be reproduced with specific athletic activities and relieved with rest.
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rotation while the examiner palpates the ipsilateral radial pulse (Fig. 27-4). Again, elimination or diminution of the pulse with reproduction of symptoms is considered a positive test result. As originally described, the Wright maneuver was believed to reproduce compression of the axillary artery in the subcoracoid region under the pectoralis minor muscle. In the Roos stress test,22 both shoulders are placed in 90 degrees of abduction and external rotation and the patient is asked to open and close the hands for several minutes. Reproduction of symptoms with pain, paresthesia, or a sense of heaviness is considered a positive test result. In the costoclavicular maneuver, the patient thrusts both shoulders downward and backward, similar to a military brace position (Fig. 27-5). This maneuver decreases the space between the first rib and clavicle, with reproduction of symptoms in a positive test.
A careful neurovascular examination of the neck, shoulder girdle, and upper extremity should be performed. Subtle findings on inspection may include scapular ptosis, trapezial atrophy, and a more horizontally oriented clavicle. The supraclavicular fossa can demonstrate tenderness to palpation, and Tinel’s sign over the brachial plexus can sometimes be elicited. Detailed manual muscle testing may reveal weakness of the interossei and hypothenar musculature. Most patients have no sensory deficits, although sometimes hypesthesia and hypalgesia are found in the little finger, hypothenar eminence, and medial aspect of the forearm.38 Some classic but nonspecific tests for thoracic syndrome are the Adson test,24 the Wright maneuver,14 the Roos, or overhead stress test,22 and the costoclavicular maneuver. During the Adson test,24 the patient extends the neck, turns the head toward the affected shoulder, and inhales deeply (Fig. 27-3). The examiner palpates the ipsilateral radial pulse with the patient’s arm lying at his or her side. Elimination or diminution of the pulse while simultaneously reproducing the patient’s symptoms constitutes a positive test result. This test was originally believed to be pathognomonic for scalenus anticus syndrome. In the Wright maneuver,14 the affected arm is brought into progressive hyperabduction and external
Although these classic provocative maneuvers are often performed during the examination of the patient with suspected thoracic outlet syndrome, they are not specific. Studies have demonstrated obliteration of the radial pulse in asymptomatic subjects during the Adson, Wright, and costoclavicular maneuvers.40,41 Rayan and Jensen41 have performed provocative maneuvers in 200 extremities in 100 asymptomatic volunteers and found a vascular response present in 27 extremities during the Adson maneuver (13.5%), 114 extremities for the Wright maneuver (57%), and 94 extremities for the costoclavicular maneuver (47%). The neurologic response was present in 4 extremities for the Adson maneuver (2%), 33 extremities for the Wright maneuver (16.5%), and 20 extremities for the costoclavicular maneuver (10%). Thus, each test result should only be considered positive if it reproduces the patient’s symptoms.
Figure 27-3. The Adson test.
Figure 27-4. The Wright, or hyperabduction, maneuver.
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Figure 27-5. The costoclavicular maneuver.
The diagnosis of thoracic outlet syndrome remains clinical, although ancillary studies can provide additional information. Cervical spine radiographs should be obtained in all patients to evaluate for cervical spondylolysis, because cervical radiculopathy can mimic symptoms of thoracic outlet syndrome. Radiographs should also be inspected for the presence of cervical ribs (Fig. 27-6), elongated C7 transverse processes, and irregularities of the clavicle or first rib. A chest radiograph may reveal evidence of a Pancoast tumor that is causing referred shoulder pain. Magnetic resonance imaging (MRI) of the cervical spine is warranted if symptoms are primarily consistent with cervical nerve root compression. MRI of the thoracic outlet has recently been described to evaluate for evidence of brachial plexus compression or structural pathology,42-44 although some clinicians have not found MRI to be helpful in the diagnosis.45 Electrodiagnostic studies, including somatosensory evoked potentials, electromyography (EMG), and nerve conduction velocities have also been used to help determine the diagnosis. Brachial plexus compression is often intermittent and positional; thus, there are usually no fixed neurologic deficits that can be identified.46 Electrodiagnostic studies are helpful in the examination of a patient with a suspected concurrent or isolated lesion of a peripheral nerve.47 Vascular evaluation with arterial angiography or venography should be limited to cases with strong evidence of serious vascular pathology, such as acute subclavian or axillary artery occlusion or effort thrombosis. Ancillary tests, in conjunction with the clinical presentation and physical examination, are useful for narrowing the differential diagnosis, which includes cervical
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Figure 27-6. Radiographic demonstration of a cervical rib.
spine pathology, ulnar neuropathy, carpal tunnel syndrome, brachial neuritis, supraclavicular fossa or lung pathology, reflex sympathetic dystrophy, cardiac disease, and glenohumeral instability.18,38 The initial treatment for thoracic outlet syndrome is almost always nonoperative as long as there is no severe limb-threatening vascular compromise. An exercise program focused on correction of postural abnormalities and strengthening of the shoulder girdle and scapular musculature is essential. It is important that exercises involving shoulder bracing and overhead activity be avoided because they may aggravate symptoms.15,18,20,48 Other principles of nonoperative management include relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), weight reduction, if indicated, and avoidance of precipitating activities. In the first report of thoracic outlet compression in athletes, Strukel and Garrick in 1978 successfully treated four athletes conservatively to allow safe return to competition.32 Most cases of thoracic outlet syndrome may be successfully treated conservatively; however, there are certain cases that do require surgical intervention for optimal treatment. The most common indication for surgical management of thoracic outlet syndrome is failure of a carefully supervised postural re-education and exercise program. Other
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indications include impending vascular compromise of the extremity, intractable pain after exhaustion of every measure of conservative treatment, and the presence of a significant neurologic deficit, such as severe intrinsic wasting of the hand.38 Many different surgical procedures have been described, including scalenotomy, pectoralis minor tenotomy, claviculectomy, first rib resection, resection of cervical ribs or fibromuscular bands, or combinations of these procedures. Although there is controversy regarding the optimal surgical procedure and approach, the most commonly performed operation is a transaxillary first rib resection, with decompression of the thoracic outlet. Because of the many procedures and approaches described, lack of a standardized evaluation, and reports of mixed patient populations, it is difficult to determine the true outcomes of thoracic outlet surgery, especially in athletes.31 Most surgeons report good to excellent results, with emphasis on proper diagnosis and patient selection.
Axillary Artery Occlusion and Aneurysm The axillary artery is the main artery of the upper extremity and originates as a continuation of the subclavian artery at the lateral margin of the first rib. The artery has six primary branches and is divided into three parts based on its relation to the pectoralis minor muscle (Fig. 27-7). The first part is proximal to the muscle; this includes the superior thoracic artery. The second part is posterior to the muscle and has the thoracoacromial and lateral thoracic artery
1 2 3
Axillary artery Pectoralis minor muscle
Figure 27-7. Anatomy of the axillary artery. The first part is proximal to the pectoralis minor muscle (1), the second part is posterior to the muscle (2), and the third part is located distal to the muscle (3).
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branches. The third part is located distally to the pectoralis minor; this includes the anterior and posterior humeral circumflex and subscapular arteries. In 1945, Wright described a “hyperabduction syndrome,” in which the second part of the axillary artery was occluded by the overlying pectoralis minor muscle when the arm was brought overhead.14 Tullos and associates,49 in 1972, were the first to report on a major league pitcher with axillary artery occlusion. They postulated that in the cocking phase of pitching, the arm is brought into abduction, extension, and extreme external rotation, with resultant transient occlusion of the axillary artery by a stretched pectoralis minor muscle. Over time, with the repetitive trauma of pitching, enough injury was inflicted to produce intimal damage and subsequent thrombosis. The pectoralis minor and humeral head have been shown to be hypertrophied in pitchers.50,51 Such structures might be more prone to compress adjacent neurovascular structures. McCarthy and coworkers,52 in their report on 11 athletes with thoracic outlet compression, have noted compression of the subclavian and axillary arteries and their branches by hypertrophied anterior scalene and pectoralis minor muscles; the 6 baseball pitchers treated with anterior scalene or pectoralis minor resection all returned to competition. Other clinicians have documented compression of the third part of the axillary artery by the humeral head. Using duplex Doppler scanning, Rohrer and colleagues53 have demonstrated that with the arm in the throwing position, the axillary artery is compressed by the humeral head in 83% of the 92 arms examined; however, there is more than 50% stenosis in only 7.6% of arms. It was concluded that this intermittent compression of the axillary artery by the humeral head predisposes the throwing athlete to axillary artery thrombosis. In conjunction with thrombosis of the axillary artery, there have been many reports describing aneurysms of the axillary artery and its branches in overhead athletes.49,52-59 The humeral circumflex arteries encircle the surgical neck of the humerus and tether the axillary artery in a fixed position relative to the humerus. In the throwing motion, with downward displacement of the humeral head during abduction and external rotation, the axillary artery can become compressed proximally or stretched at its junction with the humeral circumflex arteries. Repeated compression can lead to intimal damage and thrombosis, and such repetitive stretching can lead to aneurysmal formation.54,60,61 Affected patients may complain of nonspecific symptoms of pain, intermittent paresthesia, digital pain, arm heaviness, and cold intolerance. The well-conditioned athlete may present initially with easy fatigability, loss of pitching velocity, loss of arm control, and the dead arm syndrome. On physical examination, the clinician may note signs of digital ischemia, such as ulcers, sluggish capillary refill of the digits, coolness to the affected extremity, and tenderness about the
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pectoralis minor. The physician should attempt to palpate pulses and auscultate for bruits in the patient’s arm in the neutral and functional positions. Placing the arm in abduction and external rotation can sometimes reproduce symptoms. In addition to a detailed history and physical examination, the diagnosis requires a high index of suspicion and other ancillary studies. Noninvasive tests for vascular pathology include duplex Doppler scanning, pulse volume recording, and digital photoplethysmography.61 The definitive test is positional angiography to define the arterial anatomy clearly, identify areas of compression, occlusion, and aneurysm formation, and evaluate the distal arterial architecture for sites of embolization. Nonoperative treatment is generally not effective for axillary artery compression and aneurysm. Anticoagulation has been used primarily as an adjunct to surgical intervention but has sometimes been used as the sole therapy. Rohrer and associates53 have treated a major league pitcher with axillary artery thrombosis with an intra-arterial urokinase infusion, followed by aspirin and dipyridamole. Recurrent occlusion was treated with a similar course of urokinase followed by warfarin (Coumadin). Maintenance therapy with subcutaneous heparin injections after pitching outings allowed resumption of his career, with no further episodes. Common surgical options include sympathectomy, decompression with muscle resection, and various vascular reconstructive procedures.49,52,57,61,62 Tullos and coworkers49 initially performed a transthoracic cervical sympathectomy on a major league pitcher with complete occlusion of the axillary artery. He was able to pitch effectively for almost 2 years until recurrence of symptoms required a subclavian to brachial artery bypass graft. In the vascular and orthopedic literature, McCarthy52 and Nuber57 and colleagues have reported on a group of athletes with symptomatic compression or occlusion of the subclavian or axillary arteries and their branches. Patients with subclavian aneurysms were treated with a saphenous vein bypass graft and cervical rib resection. The athletes with muscular compression were treated with resection of the anterior scalene, pectoralis minor muscles, or both. Specific arterial branch compressions were freed with dissection. All pitchers except one were able to return to their previous levels of competition. In the presence of an aneurysm, surgical options include bypass grafting and segmental resection with patching or primary anastomosis. Todd and associates60 have reported on two major league pitchers with symptomatic aneurysms of the axillary artery at the origin of the circumflex humeral arteries who were successfully treated with resection and reversed saphenous vein interposition graft. Arko and coworkers63 published their results of treatment of vascular complications in high-performance athletes. Seven patients, including five pitchers, one volleyball player, and one cyclist had aneurysms of the proximal upper extremity arteries. The five athletes with arteriographic evidence of significant distal
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embolization underwent preoperative lytic therapy. Six patients underwent operative intervention with resection— lateral arterial repair with vein patch angioplasty in four patients, and resection and reversed saphenous vein interposition graft in the remaining two patients. All six arterial reconstructions remained patent at a mean follow-up of 42.2 months, with each patient returning to competition without recurrent symptoms. Case reports of major league pitchers with aneurysms of axillary artery branches, who presented with digital ischemia of their pitching hands as a result of embolic phenomenon, have documented successful return to competition after resection and arterial repair.55,61 Ishitobi and colleagues62 have performed extra-anatomic bypass grafting with a reversed saphenous vein graft anterior to the pectoralis minor muscle and posterior to the pectoralis major muscle in four Japanese baseball pitchers with axillary artery occlusion. All pitchers were able to continue pitching for 3 to 9 more years of competition. Long-term evaluation demonstrated normally functioning bypass grafts. Pitchers and other overhead athletes with complaints of early fatigue, claudication-type symptoms, or evidence of emboli require an early complete examination for axillary artery injury and prompt institution of appropriate therapy. Failure to recognize this disorder can lead to disastrous and catastrophic consequences. Fields and associates64 have reported on a major league pitcher who sustained a stroke, likely from retrograde propagation of a thrombus, with resultant complete occlusion of the innominate artery.
Effort Thrombosis The axillary vein originates at the lower border of the teres major muscle as a continuation of the basilic vein and becomes the subclavian vein at the lateral margin of the first rib. The axillosubclavian vein courses through a tunnel formed by the first rib posteroinferiorly, the clavicle and subclavius muscle anteriorly, the scalenus anticus muscle laterally, and the costoclavicular ligament medially.65 Compression of the axillosubclavian vein can occur at a number of locations along its anatomic course. The most commonly proposed site of compression is the costoclavicular space between the first rib and either the scalenus anticus muscle, clavicle, or costoclavicular ligament (Fig. 27-8).66 The costoclavicular space can be further narrowed by shoulder depression and especially by humeral abduction and external rotation. Described in separate publications by Paget in 187567 in London and Von Schroetter in 188468 in Vienna, primary or spontaneous thrombosis of the axillosubclavian vein typically affects young, healthy, athletic individuals. PagetSchroetter syndrome has also been called effort thrombosis because of its common association with repetitive or strenuous upper extremity activities.69-72 It has been theorized that chronic intermittent compression of the affected portion of the vein leads to intimal damage and subsequent inflammation and thrombosis.73 Effort thrombosis
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Costoclavicular compression area
Subclavian vein
Clavicle
1st rib
Axillary vein Figure 27-8. Anatomy of the axillosubclavian vein.
has been reported in many athletes, including football players,63 swimmers,74 hockey players,75 wrestlers,76 weightlifters,73 volleyball players,77 and elite pitchers in baseball.78 Although axillary vein thrombosis represents only 2% of all deep venous thrombosis cases, effort thrombosis is probably the most common vascular problem in athletes.79 Affected patients typically will give a history of strenuous or repetitive overhead activity before the onset of symptoms. Patients will complain of a feeling of arm heaviness or tiredness, dull aching pain, paresthesia, and easy fatigability during activities involving the extremity. On physical examination, the clinician may note swelling of the entire upper extremity with mottled, cool skin and dilated, prominent superficial veins (Fig. 27-9). Pulses are usually normal and symmetrical, although they may become diminished with the costoclavicular, Adson,24 and Wright14 maneuvers. The neurologic examination is normal, although nondermatomal hyperesthesia may be documented. Occasionally, tender cords may be palpated in the axilla. These physical signs may become even more
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pronounced when the patient is instructed to perform exercise tests or overhead activities. 20,77,78,80 The diagnosis of effort thrombosis is often made with a complete history and physical examination; it is confirmed with venography demonstrating occlusion or substantial narrowing of the axillosubclavian vein in the area of the clavicle and first rib (Fig. 27-10). Venography must be considered the gold standard test for diagnosis.81 Treat and coworkers77 have discussed the role of Doppler ultrasound versus venography and determined that Doppler studies have limited use in the evaluation of patients with effort thrombosis. Additionally, some physicians have advocated serologic screening for a possible hypercoagulable state.78 The goals in treatment of Paget-Schroetter syndrome of the athlete include immediate relief of the venous obstruction, correction of any predisposing anatomic abnormalities, prevention of recurrent thrombosis, and a safe return to competition.82 Historically, patients with effort thrombosis were treated nonoperatively with bed rest, arm elevation, and anticoagulation with heparin and warfarin.69,70,78,83-85 However, many reports have documented a high rate of disabling residual symptoms with this treatment. Adams and DeWeese,84 in 1971, noted late residual symptoms of swelling, pain, and superficial thrombophlebitis in 68% of patients and a troubling 12% incidence of pulmonary embolism. The presence of these persistent symptoms has led to more aggressive treatment. Currently, management of effort thrombosis includes a multidisciplinary approach with venography, followed by thrombolytic therapy and surgical decompression of the thoracic outlet. Many reports have documented the efficacy of early thrombolytic therapy with streptokinase or urokinase.65,69,73,78,81,83,86-89 Through venography and thrombolysis, it was discovered that most patients had compression of the axillosubclavian vein in the costoclavicular space, which was accentuated with humeral abduction and external rotation.70,73,87 Whereas venous thrombosis occurs
B
A
Figure 27-9. Vein dilation. A, Shoulder. B, Arm.
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Figure 27-10. Venogram showing effort thrombosis.
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in 1.5% to 12% of patients with thoracic outlet syndrome, approximately 80% of patients with Paget-Schroetter syndrome have thoracic outlet compression.90 Surgical decompression of the thoracic outlet has been recommended for these patients. The risk for subsequent thrombosis is increased from recurrent compression on the vein causing repeated intimal injury, venous stasis, and a transient hypercoagulable state.89 Controversy exists about the optimal approach and timing of surgical decompression for these patients. Some clinicians have advocated a transaxillary approach with first rib resection and division of the scalenus anticus muscle,65,82,89 whereas others have advocated a supraclavicular approach.63,70 Early surgery is recommended by some who believe that thrombolysis, followed by prompt surgical decompression, should be considered the standard of care in the management of effort thrombosis.65,70,82 Others prefer the traditional staged approach of thrombolysis, followed by an intervening period of anticoagulation before surgical decompression.89 It is critical that thrombolysis therapy be instituted promptly. Numerous reports have demonstrated the efficacy of acute intervention and treatment with superior results compared with delayed intervention.65,91,92 Patients with Paget-Schroetter syndrome can expect excellent clinical results with a low rate of residual symptoms with an early diagnosis, thrombolysis and, if indicated, thoracic outlet decompression.89 Even though the syndrome is rare, athletes who perform repetitive and vigorous upper extremity activities are at risk for developing effort thrombosis. Physicians should be familiar with the signs and symptoms associated with this condition so that appropriate therapy may be instituted early.
Quadrilateral Space Syndrome The quadrilateral, or quadrangular space, is located over the posterior scapular and subdeltoid regions. The boundaries include the teres minor superiorly, the long head of the triceps medially, the teres major inferiorly, and the surgical neck of the humerus laterally (Fig. 27-11). The neurovascular bundle, consisting of the axillary nerve and posterior humeral circumflex artery, passes through the space. In a critical review of the results of thoracic outlet syndrome surgery, many failures were noted that seem to have the common denominator of occlusion of the posterior humeral circumflex artery in the position of abduction and external rotation.93,94 Further investigations have led to the description of quadrilateral space syndrome. This syndrome is an uncommon neurovascular compression syndrome, primarily affecting young active adults.95 Patients usually present with complaints of intermittent, poorly localized anterior shoulder pain. Concurrent paresthesia typically radiates in a nondermatomal distribution. Symptoms are aggravated with forward flexion, abduction, and external rotation. There is usually no
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Surgical neck of humerus
Teres minor m. Teres major m.
Axillary nerve
Posterior humeral circumflex artery Quadrilateral space Long head of triceps m. Figure 27-11. Anatomy of the quadrilateral space.
history of a specific injury, although the syndrome may be associated with chronic repetitive stress to the shoulder.95,96 On physical examination, discrete point tenderness is found posteriorly over the quadrilateral space.94 Symptoms are usually reproduced with the patient’s arm held flexed, abducted, and externally rotated for 1 minute. The neurologic examination and electrodiagnostic study results are usually normal, although sometimes deltoid atrophy may be seen.97 The definitive diagnosis is made with a subclavian arteriogram. The arteriogram is obtained with the arm held at the patient’s side and in an abducted, externally rotated position. In affected patients, the arteriogram will show a patent posterior humeral circumflex artery with the humerus at the side, but reveals occlusion of the artery when the humerus is abducted and externally rotated (Fig. 27-12). Magnetic resonance angiography has not been shown to have value in the diagnosis of quadrilateral space syndrome,98 and MRI findings demonstrating selective atrophy of the teres minor are only suggestive of the diagnosis in the appropriate clinical setting.99 There have been case reports of quadrilateral space syndrome caused by a paralabral cyst or ganglion as seen on MRI scans.100,101 Once the definitive diagnosis has been made, the initial treatment is nonoperative and includes rest, reassurance, symptomatic care, and physical therapy. Gentle internal rotation stretching of the glenohumeral joint, horizontal stretching into adduction, and posterior rotator cuff strengthening may help alleviate symptoms.80 Redler and associates102 have reported on a baseball pitcher who experienced symptomatic relief and continued pitching after changing
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A
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B
Figure 27-12. Arteriograms showing compression of posterior humeral circumflex artery. A, Patient’s arm at side. B, Patient’s arm abducted.
his delivery from an overhead to a three-quarters overhead pitching motion. On average, 30% of patients will have continued symptoms, despite appropriate conservative treatment, that warrant surgical management.94,95 Reports of operative treatment have consisted largely of small patient series.94-96,103 In the largest report to date, Cahill and Palmer94 have described 18 patients whom they treated operatively with decompression of the quadrilateral space through a posterior approach. At surgery, they discovered obliquely oriented fibrous bands filling the space and tethering the neurovascular bundle. After the fibrous bands were released, decompression was deemed to be adequate when the posterior humeral circumflex artery pulse remained palpable in the position of abduction and external rotation. Of these 18 patients, 16 had partial or complete resolution of symptoms. Symptoms were believed to arise from compression of the axillary nerve and its afferent fibers by the fibrous bands. The origin of these fibrous bands remains unknown, and Cahill and Palmer were unable to identify these bands in cadavers. It has been theorized that normal structures in the quadrilateral space may fibrose and scar after chronic repetitive overhead activity, resulting in pathologic anatomy and compression.20,95
SUMMARY Although relatively rare, neurovascular compression syndromes of the shoulder can be a significant cause of disability and can prevent an athlete from performing at his or her highest level. Early diagnosis and institution of therapy require a detailed history and physical examination, a high index of suspicion, and selective use of ancillary studies. With appropriate treatment, most athletes are able to return to sports successfully.
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References 1. Tyson RR, Kaplan GF: Modern concepts of diagnosis and treatment of the thoracic outlet syndrome. Orthop Clin North Am 6:507-519, 1975. 2. Coote H: Pressure on the axillary vessels and nerve by an exostosis from a cervical rib: Interference with the circulation of the arm, removal of the rib and exostosis; recovery. Med Times Gazette 2:108, 1861. 3. Murphy JB: A case of cervical rib with symptoms resembling subclavian aneurysm. Ann Surg 41:398-406, 1905. 4. Keen W: The symptomatology, diagnosis, and surgical treatment of cervical ribs. Am J Med Sci 133:173, 1907. 5. Stopford JSB, Telford ED: Compression of the lower trunk of the brachial plexus by a first dorsal rib with a note on the surgical treatment. Br J Surg 7:168, 1919. 6. Wheeler WI: Compression neuritis due to the normal first dorsal rib. Practitioner 104:409, 1920. 7. Brickner WM, Milch H: First dorsal simulating cervical rib by maldevelopment or by pressure symptoms. Surg Gynecol Obstet 40:38, 1925. 8. Adson AW, Coffey JR: Cervical rib: A method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann Surg 85:839-857, 1927. 9. Ochsner A, Gage M, DeBakey M: Scalenus anticus (Naffziger) syndrome. Am J Surg 28:696-699, 1935. 10. Naffziger FC, Grant WT: Neuritis of the brachial plexus, mechanical in origin: The scalenus syndrome. Surg Gynecol Obstet 67:722, 1938. 11. Lewis T, Pickering G: Observations upon maladies in which the blood supply to the digits ceases intermittently or permanently. Clin Sci 1:327, 1934. 12. Eden JC: Vascular complications of cervical ribs and first thoracic rib abnormalities. Br J Surg 27:105, 1939. 13. Falconer MA, Weddel G: Costoclavicular compression of the subclavian artery and vein. Relation to the scalenus anticus syndrome. Lancet 2:539, 1943. 14. Wright IS: The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J 29:1-19, 1945.
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CHAPTER 28 Brachial Plexus Injuries Tandy R. Freeman and William G. Clancy, Jr.
Athletic injuries to the brachial plexus and peripheral nerves about the shoulder are most commonly seen in contact sports, such as American football. Hirasawa and Sakakida1 have reported that among 1176 cases of peripheral nerve and brachial plexus injuries treated over an 18-year period, only 66 were related to sports. Of these, 16 were compression injuries to the brachial plexus. They also noted a report by Takazawa and colleagues2 of only 28 peripheral nerve injuries among 9550 sports injuries seen over 5 years. In contrast to these Japanese studies, Clarke3 has reported the incidence of brachial plexus injury in U.S. high school and college football players over a 4-year period to be 2.2 injuries per 100 players per year. Clancy and associates4 have noted a 30% to 50% incidence of transitory brachial plexus injuries over the course of high school or college career. Peripheral nerve injuries, although rare, tend to be more prevalent than brachial plexus injuries in sports other than football and wrestling, especially in noncontact sports.1 Prompt recognition, appropriate assessment, and proper treatment are essential for the safe and timely return of the injured athlete to participation.
Neurotmesis is an injury in which not only is the axon disrupted, but there is also loss of the integrity of the supporting stroma of the nerve, including the endoneurium. Nonoperative recovery is unlikely because of loss of continuity of the neural tube and, even with surgical repair or reconstruction, complete return of function is unlikely. Electromyographic studies have shown denervation patterns at 3 weeks and at 1 year or later.
ANATOMY An understanding of the anatomy of the brachial plexus is essential for establishing an accurate diagnosis and prognosis in brachial plexus injuries. The brachial plexus is formed in the neck from the ventral rami of cervical nerve roots V through VIII and the first thoracic nerve root and lies between the anterior and middle scalene muscles. It passes over the first rib and deep to the sternocleidomastoid and clavicle in its course. It may receive contributions from C4 (prefixed plexus) or T2 (postfixed plexus). The ventral (motor) and dorsal (sensory) roots at each level unite near or within the vertebral foramen to form the nerve roots (Fig. 28-2). The cell bodies of the sensory nerves in the dorsal root are located in the dorsal root ganglia, situated just proximal to the confluence of the ventral and dorsal roots and outside the spinal cord. Injury proximal to the dorsal ganglion—preganglionic lesion or root avulsion—is, at this time, irreparable and has a hopeless prognosis. Injury distal to the dorsal ganglion, postganglionic lesion, represents a peripheral nerve injury with the potential for recovery spontaneously or with surgical repair or reconstruction.
CLASSIFICATION OF NERVE INJURIES Seddon5 has classified peripheral nerve injuries based on the degree of injury, correlating histologic and clinical findings with prognosis. Injury may result in varying amounts of damage to neural fibers within a given nerve, producing a mixed clinical picture based on this classification system. Neurapraxia represents a physiologic interruption of nerve function without anatomic axonal disruption. Demyelination may occur,6-8 but repair is rapid. Function returns from within minutes to 3 weeks of injury, and neurophysiologic studies are normal at that time. Axonotmesis is an injury resulting in axonal disruption without significant injury to the supporting stroma, including the endoneurium, perineurium, and epineurium (Fig. 28-1). Wallerian degeneration of the axon occurs distally and, to some extent, proximally to the level of injury, but the neural tube remains intact. Return of function requires complete regeneration of the axon, which is facilitated by intact fascicles. Electromyographic studies at 3 weeks have revealed fibrillations and positive sharp waves, with loss of motor unit potentials in the denervated muscles. After recovery, the electromyogram (EMG) may show large motor unit potentials.
Just distal to the confluence of the ventral and dorsal roots, and as the nerve root exits the vertebral foramen, the root divides into ventral and dorsal rami. The ventral rami are larger and form the brachial plexus. The smaller dorsal rami innervate the paraspinal musculature and provide sensation dorsally. The ventral rami unite just above the clavicle to form the three trunks—upper (C5 to C6), middle (C7), and lower (C8 to T1; Fig. 28-3). The site of confluence of C5 and C6 is known as Erb’s point. Between the takeoff of the dorsal rami and Erb’s point, the long thoracic nerve (serratus anterior) arises from C5 through C7, and the dorsal scapular 337
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Vessel Epineurium Perineurium
medial brachial cutaneous, and medial antebrachial cutaneous nerves arise from the cords. The cords terminate in the five terminal branches—the musculocutaneous, axillary, radial, ulnar, and median nerves.
Endoneurium
Fascicle
Nerve fiber
High-Velocity Injuries
Endoneurium Perineurium
Group of fascicles
Epineurium
Figure 28-1. Cross-sectional anatomy of a peripheral nerve. (From Wilgis EFS, Brushart TM: Nerve repair and grafting. In Green DP [ed]: Operative Hand Surgery, 3rd ed. Churchill Livingstone, New York, 1993, p 1315.)
nerve (rhomboids) arises from C5. The suprascapular nerve (supraspinatus, infraspinatus) arises distal to Erb’s point from the upper trunk. Postganglionic injury of C5 to C6 proximal to Erb’s point represents a peripheral nerve root injury, with loss of C5 to C6 paraspinous, serratus anterior, and rhomboid function. This distinguishes nerve root injuries from upper trunk injuries, which leave dorsal rami, long thoracic, and dorsal scapular nerve functions intact.
